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Semester 2 (3rd year) > case 23: health behaviours, diabetes and endocrine disease > Flashcards

case 23: health behaviours, diabetes and endocrine disease Flashcards

1
Q

by which organ and cells is insulin produced

A

beta cells in the islets of langerhans of the pancreas

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2
Q

what is C peptide

A

is by-product of insulin production and is used as a measure of endogenous insulin

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3
Q

which process does glucagon inhibit

A

glycolysis

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4
Q

process of thyroid hormone being released

A

hypothalamus realises TRH which stimulates pituitary

pituitary releases TSH which stimulates the thyroid

thyroid releases T3 and T4

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5
Q

Qs for itchy penis

A

pain
discharge
dysuria
itching/burning
sexual history
testicular swelling
lymph node swelling in groins
history of trauma/previous surgery

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6
Q

proper name for penis thrush

A

candidal balanitis

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7
Q

rfs for candidal balanitis

A

diabetes mellitus
oral abx
poor hygiene
immunosuppression

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8
Q

normal blood sugar levels

A

4-7mmol before meals

less than 9mmol 2hrs after meals

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9
Q

glucose criteria for diagnosing diabetes

A

in symptomatic:
fasting glucose greater than or equal to 7mmol
random glucose greater than or equal to 11.1

if asymptomatic above criteria must be met on 2 separate occasions

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10
Q

HbA1C criteria for diagnosing diabetes

A

if asymptotic- 48 or above

if asymptomatic- need 2 separate readings which are 48 or above

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11
Q

under which conditions would you mot use HbA1C to diagnose diabetes

A

under 18s

pregnant/2 months postpartum

symptoms for less than 2 months

high diabetes risk who are acutely ill

on medication (long-term corticosteroids) which increase hyperglycaemia risk

acute pancreatic damage (including surgery)

end stage renal disease

HIV

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12
Q

hallmark symptoms of T2D

A

tiredness

polyuria/polydypsia

recurrent infections (thrush)

increased hunger

unintentional weight loss

blurred vision (retinopathy)

foot ulcers/sores (peripheral neuropathy)

areas of dark skin for example in armpits/neck (acanthuses nigricans)

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13
Q

risk factors for T2D

A

family history

high BMI

high sugar and fat diet

inactivity

afro-caribbean, hispanic, asian

hyperlipidaemia

over 45

history of gestational diabetes

other conditions which cause insulin resistance- PCOS, haemachromatosis

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14
Q

what do alpha cells in the islets of langerhan produce

A

glucagon

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15
Q

role of insulin

A

reduces amount of glucose in blood

binds to its receptors on adipose tissue/muscle

this makes glucose transporter fuse with the cell membrane

glucose is then transported into the cell

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16
Q

role of glucagon

A

increases the amount of glucose in the blood

stimulates the liver to do gluconeogenesis and glycolysis

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17
Q

is T1D or T2D more common

A

10%= 1
90%= 2

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18
Q

what type of hypersensitivity is T1D

A

type 4- T cells attack the pancreas

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19
Q

where genetically is the issue in T1D

A

on chromosome 6, major histocompatibility complex (MHC), human leukocyte antigen (HLA 3 and 4)

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20
Q

other name of hunger

A

polyphagia

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21
Q

what causes weight loss and hunger in diabetes

A

lack of glucose in muscle and adipose tissue

adipose tissue undergoes lipolysis

muscle breaks down into proteins

causes weight loss and hunger

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22
Q

what causes polyuria in diabetes

A

increased glucose in blood means more filtered by kidneys and more in urine

glucose is osmotically active so draws water with it

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23
Q

what causes polydipsia in diabetes

A

the excess water loss leads to dehydration and therefore thirst

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24
Q

process of DKA

A

there is lipolysis of adipose tissue meaning increases fatty acids

the liver converts these to ketone bodies

ketones bodies can be used for energy but they also increase the acidity of the blood- ketoacidosis

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25
Q

what type of respiration may be seen in DKA

A

kussmaul breathing- this is a deep laboured breathing to reduce CO2 and reduce the acidity of the blood

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26
Q

what electrolyte abnormality may be observed in DKA

A

hyperkalaemia

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27
Q

what happens to the ions in DKA

A

there is a high anion gap (large difference in unmeasured ions)

this is due to the ketoacid buildup

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28
Q

what causes fruity breath in DKA

A

acetone

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29
Q

treatment of DKA

A

fluids for dehydration
insulin to lower blood glucose
electrolytes (K+)

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30
Q

what happens to the beta cells in T2D

A

there is hyperplasia and hypertrophy

(this is due to the body producing insulin but there being no response as cells don’t reposed, therefore the body increases beta cells to make more insulin)

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31
Q

amyloid deposits and T2D

A

the beta cells also make islet amyloid polypeptide (amylin)

hyperplasia and hypertrophy of beta cells mean more amylin- leads to amyloid deposits

the maxed out beta cells can then undergo hypotrophy and hypoplasia

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32
Q

pathophysiology of HHS

A

when glucose is very high in blood (hyperosmolar state) water goes from the bodies cells meaning they shrivel

blood vessels which are full of water lead to increased urination which leads to total body hydration

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33
Q

overlap between HHS and DKA

A

in HHS there is sometimes mild ketonemia and acidosis

in DKA there may be some hyperosmolarity

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34
Q

is DKA/HHS more common in type 1 or 2 diabetes

A

DKA= more common in 1
HHS= more common in 2

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35
Q

what trimester is most commonly affected by gestational diabetes

A

3rd

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36
Q

what is checked at an annual diabetic review

A

BP
eye tests
foot examination
blood sugars
urine
HbA1c
height and weight
cholesterol

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37
Q

diet and lifestyle management of T2D

A

initial weight loss target of 5-10%

reduce alcohol

stop smoking

encourage exercise (150-300mins of moderate intensity aerobic exercise per week)

eat carbohydrates from vegetables, pulses, and whole grains

eat low fat dairy products and oily fat

limit foods with saturated fats/trans fatty acids

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38
Q

when do you give medication for T2D

A

HbA1C is checked every 3-6months until stable
if lifestyle has failed and is 48 or higher, consider medication

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39
Q

how does metformin work

A

it is a biguanide
leads to activation of AMP-activated protein kinase (AMPK)
this increases insulin sensitivity and decreases hepatic gluconeogenesis

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40
Q

most common side effect of metformin

A

GI disturbance (taking with meals/metformin MR can reduce this)

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41
Q

2nd line medication for T2D if metformin isn’t reducing HbA1C

A

SGLT2 inhibitors (flozin)

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42
Q

when would you consider insulin therapy in T2D

A

if using 3 medications and HbA1C still not controlled

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43
Q

drugs which reduce insulin resistance in T2D

A

biguanides (metformin)
thiazolidenediones (pioglitazone)

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44
Q

drugs which increase beta cell activity in T2D

A

sulphonylureas (gliclazide, glipizide)
meglitinides (nateglinide, repaglinide)

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45
Q

drugs which increase GLP1 activity in T2D

A

DPP4 inhibitors (sitagliptin, vildagliptin)
incretins, GLP1 agonists (exenatide, liraglutide)

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46
Q

drugs which enhance glucose secretion in T2D

A

SGLT2 inhibitors (dapaflozin, canagliflozin)

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47
Q

drugs for T2D which can cause weight gain

A

sulphonyureas
meglitinides
insulin

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48
Q

drugs for T2D which can cause hypoglycaemia

A

sulphonyureas
meglitinides
insulin

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49
Q

drugs for T2D which can cause GI disturbance

A

metformin
incretins
acarbose

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50
Q

drugs for T2D which can cause weight loss

A

metformin
SGLT2 antagonists
incretins

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51
Q

which T2D drug can be associated with osteoporosis

A

pioglitazone

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52
Q

what other side effect can SGLT2 inhibitors be linked to

A

UTIs

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53
Q

what hypertension drug class is first line for all diabetes

A

ACE inhibitors

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54
Q

when would you give statins with diabetes

A

recommended in most T1D
recommended in T2D if QRISK greater than 10%

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55
Q

what is the blood pressure target for diabetes

A

below 140/80

below 130/80 if there is end organ damage (kidneys, eyes etc)

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56
Q

diagnostic criteria for DKA

A

capillary blood glucose over 11 (or known diabetes)

capillary ketones over 3 (or urinary over 2)

venous pH less than 7.3 or venous bicarbonate less than 15

(must have all 3 for diagnosis)

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57
Q

at what rate do you give insulin for DKA

A

IV fixed rate insulin is at 0.1 units/kg/hr

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58
Q

K+ and insulin

A

giving insulin drips K+ (makes sense as insulin is used to manage hyperkalaemia)

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59
Q

when would you escalate DKA to critical care

A

venous bicarbonate less than 5
pH less than 7.1
drowsy GCS of less than 12
stats less than 92% on room air
K+ less than 3.5 on admission
pregnant
HF
oliguria/anuria
persistant hypotension

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60
Q

with DKA when would you change fixed rate IV insulin to subcutaneous insulin

A

when patient is eating and drinking normally
pH over 7.3 or blood ketones less than 0.6

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61
Q

effect of insulin on adipose tissue and skeletal muscle

A

increases glucose uptake
increases glycolysis

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62
Q

effect of insulin on liver

A

increases glycolysis
increases glycogenesis
increases protein synthesis
increases lipogenesis

decreases gluconeogenesis
decreases lipolysis
decreases glycogenolysis
decreases protein breakdown

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63
Q

clinical presentation of T2D

A

asymptomatic
infections
fatigue
blurred vision

4ps:
paraesthesia
polydipsia
polyuria
polyphagia

64
Q

retinopathy and T2D

A

may see:
cotton wool spots
haemorrhage
microaneurysm
macular thickening

can cause glaucoma and cataracts

65
Q

peripheral neuropathy and T2D

A

can have:
increased or decreased pain
painless injury
decreased reflexes

66
Q

autonomic neuropathy and T2D

A

can have:
resting tachycardia
urinary frequency
erectile dysfunction

67
Q

nephropathy and T2D

A

can have:
glomerulosclerosis
pyelonephritis

68
Q

macrovascular complications of T2D

A

coronary heart- chest pain, CHF, dyspnoea

cerebrovascular- haemorrhage, cerebral infarct, memory problems

peripheral vascular- atherosclerosis, gangrene, ulceration

69
Q

3 vascular changes in diabetes

A

atherosclerosis
arteriosclerosis
inflammation

(occurs due to alterations in vascular homeostasis due to endothelial and smooth muscle cell dysfunction)

70
Q

hyperglycaemia and its effect on cells in T2D

A

due to hyperglycaemia cells take up lots of glucose

this forms reactive O2 species

this forms advanced glycalated product (AGP) and protein kinase C

protein kinase C causes more reactive O2 species to be made (a cycle)

71
Q

effects of protein kinase C in T2D

A

increases VEGF and other growth factors- this causes angiogenesis and cell growth

increases endothelin- causes platelet aggregation

increases NFkappaB- is inflammatory mediator so increases inflammation and vascular permeability

the increased vascular permeability allows LDL and monocytes (which become macrophages) to come into blood

72
Q

macrophages and LDL (atherosclerosis)

A

macrophages engulfs the LDL- becomes a foam cell

foam cell releases inflammatory mediators (TNF-alpha and IL-1) which causes inflammation

73
Q

causes of DKA (the 5 is)

A

infection
intoxication
inappropriate withdrawal of insulin
intercurrent infection
infarction

74
Q

what other investigations are important for DKA

A

ABG (monitor pH)
urinalysis
FBC
ECG

75
Q

all sound women presenting with abdominal pain must have what

A

pregnancy test

76
Q

what is a basal bolus of insulin

A

long acting insulin is given as a subcutaneous injection to act as endogenous insulin (basal or base)

rapid acting insulin is given to replicate the normal response to food (bolus)

3 boluses a day are given with meals (varies depending on how may meals they’re having)

77
Q

what is a mixed bi-phasic insulin regime

A

usually one two or three insulin injections per day

they are premixed insulin preparations which contain insulins of different durations of action (slow and fast)

78
Q

what is a continuous insulin regime

A

insulin pumps can be used to deliver rapid acting insulin at a very slow rate as background insulin

mealtime insulin can be delivered by the patient according to what they eat

insulin is delivered subcutaneously via cannula- the two main types are tethered pumps or catch pumps

79
Q

where do you administer insulin injections

A

anywhere where there is subcutaneous fat (tummy, thigh, top of arm, buttocks)

80
Q

what education programme should diabetics be offered

A

DAFNE (dose adjustment for normal eating programme)

counselling on following- carbohydrate counselling, sick day rules, hypo awareness, diabetic complications and the need for screening

81
Q

how many times a day should a diabetic on insulin check their glucose levels

A

at least 4 times per day

82
Q

when are particularly important times to check your blood glucose if diabetic and on insulin

A

before each meal and before bed

83
Q

what are the blood glucose targets for diabetes

A

5-7mmol/l on waking
4-7mmol/l before meals and at other times of the day

84
Q

sick day rules for insulin check

A

blood sugars more frequently
staying hydrated
eat little and often
keep taking medications

85
Q

is the mortality for DKA or HHS higher

A

higher for HHS

86
Q

key features on blood in DKA

A

hyperglycaemia, hypovolaemia, ketonaemia and anion gap metabolic acidosis

87
Q

what causes fluid and electrolyte loss in DKA

A

there is lots of glucose in the blood

this increases the osmotic pressure

fluid shifts from intracellular to extracellular space, pulling fluid into the vasculature

leads to osmotic diuresis- causes the hypovolaemia (can lead to hypovolaemic shock)- this will also decrease the eGFR meaning the kidneys struggle to excrete glucose in the urine, furthering the problem

electrolytes follow the water

88
Q

the breakdown of what creates ketones

A

lipids

89
Q

lactic acid and DKA

A

the hypovolaemia causes poor tissue perfusion

this causes cells to switch to anaerobic metabolism

creates lactic acid as a result- this further worsens the problem of the metabolic acidosis (increases anion gap)

90
Q

how do you work out anion gap

A

Na+ + K+) - (Cl- + HCO3-)

91
Q

normal anion gap

A

4-12mmol/L

92
Q

hypokalaemia and DKA

A

because of the intracellular acidosis there is lots of K+ inside cells

to combat this, there is a shift of K+ from intracellular to extracellular

this combined with osmotic diuresis leads to low K+

administering insulin furthers this problem

93
Q

glucose levels in DKA vs HHS

A

glucose levels in HHS are typically much higher than DKA

94
Q

onset of DKA vs HHS

A

DKA= less than 24hrs
HHS= can be weeks-months

95
Q

main differences between DKA and HHS

A

no ketosis in HHS

more glucose in HHS

DKA is quicker onset

in HHS no kaussmals breathing, nausea and vomiting, ketone breath and abdominal pain

more diuresis in HHS (severe dehydration 9-10litres)

96
Q

PH in DKA vs HHS

A

DKA= acidosis
HHS= normal (if acidosis will be due to lactic acid buildup due to hypoperfusion and anaerobic respiration)

97
Q

is CNS disturbance more common in DKA or HHS

A

HHS due to the severe hypovolaemia

98
Q

management of DKA and HHS

A

treating underlying cause- could be infection

fluid replacement- 0.9% saline with (rapid bolus in 1st 1hr depending on BP and Na+), continue until fluid volume is restored

treating hyperglycaemia- IV insulin (more in HHS due to higher glucose) until normal pH (need to wean off)

electrolyte replacement- if K+ less than 5.5mmol/L

99
Q

what nail disorder is associated with graves disease

A

oncholysis (painless separation of the nail from the nail bed)

100
Q

antibodies seen in thyroid disease

A

TSH receptor antibodies- in 90% with graves

TPO antibodies- in 80% hashimotos thyroiditis

thyroglobulin antibodies- in 80% hashimotos thyroiditis

101
Q

does thyroid move on swallowing

A

yes
it is attached to thyroid cartilage and upper end of the trachea

102
Q

what cells make up the thyroid

A

cuboidal epithelium

103
Q

how are thyroid hormones made

A

they are produced by the iodination of tyrosine residues bound to thyroglobulin in thyroid follicles

iodine is taken up by the thyroid gland under the control of TSH

104
Q

is more T4 or T3 released by the thyroid gland

A

10x more T4 than T3

105
Q

3 most common causes of hyperthyroidism in UK

A

graves disease
toxic multi nodular goitre
solitary toxic adenoma

106
Q

examination findings which are specific to graves

A

exophthalmos
opthalamoplegia
thyroid acropachy
pretibial myxoedema

107
Q

what does sub-clinical hyperthyroidism look like on bloods

A

T3 and T4 normal (on high side of normal)
TSH decreased (due to negative feedback)

108
Q

thyroid eye disease symptoms and their causes

A

retraction of upper and lower lids (sympathetic override)

lid lag

swelling of eyelids/conjunctiva

exposure/dehydration of cornea (dry eye and inadequate blink coverage)

protrusion of eyeballs- exopthalamos/proptosis

double vision/squint (inflammation and fibrosis of muscles)

optic neuropathy (visual failure from optic nerve compression)

109
Q

treating thyroid eye disease

A

regular thyroid medications

artificial tears

smoking cessation

selenium

surgical intervention to improve lid closure

prisms in glasses for quint/diplopia (may need surgery eventually)

if severe or a threat to the optic nerve- high dose steroid (prednisone)/immunosupression

surgical orbital decompression

110
Q

what are the thyroid follicles filled with

A

colloid

111
Q

the 2 main cells in the thyroid gland and what they produce

A

columnar epithelium (thyroid follicular cells)- make thyroglobulin

interspersed C-cells- make calcitonin

112
Q

can TRH from the hypothalamus be measured

A

no

113
Q

what drug can result in strange TFTs

A

amiodarone (it contains lots of iodine)

114
Q

is thyroid eye disease more common in men or women

A

women but typically more severe in men

115
Q

antibodies against which growth factor receptor can be seen in thyroid eye disease

A

insulin like growth factor receptor 1

116
Q

insulin like growth factor receptor 1 antibodies effects

A

increases collagen production which builds up in tissue around the eyes

this causes fibrosis

can push on nerves, blood vessels and the eye itself

117
Q

which medication is specific for thyroid eye disease

A

teprotumumab- human monoclonal antibody which blocks IGF-1R activation (it degrades the receptors)

118
Q

what is T3 and T4s overall effect

A

increase metabolic rate

examples:
growth (of muscles)
CNS development
cardiovascular (cardiac output and HR)

119
Q

what is thyrotoxic crisis/thyroid storm

A

it is a severe acute complication of hyperthyroidism

120
Q

role of T3 specifically

A

majority of T4 is converted to T3 in the blood

T3 role:
speeds up cells basal metabolic rate- cells produce more proteins and burn more energy (fats and sugars)

increases cardiac output

stimulates bone resorption

activates sympathetic nervous system- triggers fight or flight

121
Q

why can thyrotoxic crisis/thyroid storm happen

A

more unbound thyroid hormone in the blood

tissues might become more sensitive to thyroid hormone

body might become more sensitive to catecholamines (adrenaline/dopamine)

122
Q

triggers for thyrotoxic crisis/thyroid storm

A

stressors- surgery, trauma, infection, childbirth

abruptly stopping treatment (for hyperthyroidism)

taking too much thyroid hormone (for hypothyroidism)

all of which lead to a severe state of hypermetabolism

123
Q

symptoms thyrotoxic crisis/thyroid storm

A

weight loss (despite increased appetite as metabolism is increased)

heat intolerance (body is producing more heat)- can lead to fever

tachycardia- can lead to cardiac arrhythmia and high output cardiac failure

sweating, hyperactivity, anxiety, insomnia (effect of thyroid hormone on sympathetic nervous system)- can lead to agitation, confusion seizures and coma

124
Q

diagnosis of thyrotoxic crisis/thyroid storm

A

based on severity of symptoms

on ECG can see cardiac arrhythmia

there isn’t much difference in thyroid hormone (it is to do with how the hormone is affecting the body symptoms)

125
Q

treatment for thyrotoxic crisis/thyroid storm

A

beta blockers (for symptoms)

thionamides (block thyroid hormone production)

iodine preperations

glucocorticoids

bile acid sequestrants

if the above fails can do plasmapheresis (remove plasma, take thyroid hormone out then put clean plasma back in)

126
Q

what links the hypothalamus to the anterior pituitary

A

the hypophyseal portal system

127
Q

what is the most common cause of hypothyroidism in the developing world

A

iodine deficiency (iodine is essential for thyroid hormone synthesis)

iodine is added to food such as table salt to reduce deficiency likelihood

128
Q

medications which can cause hypothyroidism

A

lithium (it inhibits thyroid hormone)

amiodarone (interfere with thyroid hormone production and metabolism)- but this one can also cause thyrotoxicosis

129
Q

central causes of hypothyroidism

A

hypopituitarism which can be due to:
tumours
infection
vascular pathology (sheehans syndrome- massive blood loss during surgery)
radiation

130
Q

fluid and hypothyroidism

A

can have oedema, pleural effusion, ascites

131
Q

what does secondary hypothyroidism look like on bloods

A

there is a problem with pituitary therefore TSH is low

because of this T3 and T4 is also low

132
Q

what are the 3 main treatment options for hyperthyroidism

A

antithyroid medication- carbimazole, methimazole, propylthiouracil

total thyroidectomy

radioactive iodine therapy

(beta blockers can manage symptoms such as anxiety tremor and palpitations)

133
Q

potential serious side effects of carbimazole

A

neutropenia (low neutrophils)

agranulocytosis (acute febrile condition marked be severe decrease in granulocytes)

134
Q

safety netting you need to do when prescribing carbimazole

A

report signs of infection (especially sore throat)- need urgent FBC

need to stop treatment if white cells are low

135
Q

smoking and hyperthyroidism

A

worsens graves disease (especially thyroid eye disease)

136
Q

pregnancy and hyperthyroid medication

A

ask if planning to conceive, check sexual history and contraception

needs to be switched to propylthiouracil if trying to conceive as carbimazole is associated with congential abnormalities

propylthiouracil in 1st trimester then switch to carbimazole from 2nd (as propylthiouracil can cause liver failure)

137
Q

what blood tests would you check before administering carbimazole

A

FBC TFTs LFTs

138
Q

monitoring bloods following prescribing mediation for thyroid disease

A

TFTs very 4-6 weeks whilst the dose is being titrated

TFTs every 3-6 months once patient is euthyroid and maintenance dose achieved

139
Q

how does radioactive iodine treatment for hyperthyroidism work

A

radioactive iodine-131 is taken orally and taken up rapidly via the thyroid gland, the release of radiation destroys the tissue over 6-18 week period

140
Q

complications of radioactive iodine

A

early complications= neck discomfort and possible precipitation of graves opthalmology (review to check)

longer term= progressive incidence of hypothyroidism, most need thyroxine after several years

141
Q

is solitary toxic nodule cancerous

A

no
it is benign

142
Q

pathological cardiovascular effect of thyrotoxicosis

A

AF- there is 3x the risk in over 60s

143
Q

how long are you treated for hyperthyroidism

A

6-24 months as if it is graves it may go into remission (but it can sill come back after redrawing drug)

144
Q

management of agranulocytosis

A

hospitalisation and antibiotics

145
Q

is there a risk of cancer with radioactive iodine 131

A

no

146
Q

does radioactive iodine 131 cause infertility

A

no, however women are advised to not get pregnant until 6 months after treatment

147
Q

what are the limitations following giving radioactive iodine-131

A

no close contact (less than 1m) with children and pregnant people for at least 9 days

after 3 weeks they can have limited contact (less than 15mins)

when using higher doses can have an adult in the same bed for at least 4 days and cant use public transport

in conclusion the limitation is up to 3 weeks after

148
Q

what is the standard surgery for hyperthyroidism

A

near-total thyroidectomy (patient takes levothyroxine after and relapse is less than 2%)

149
Q

potential complications of near-total thyroidectomy

A

it is dependant on the surgeon (if they have done more than 20 cases it is preferred)

obviously hypothyroidism is inevitable
permeant parathyroid damage (2-4%)
vocal cod paralysis (less than 1%)
bleeding (less than 2%)
keloid scars

150
Q

what is seen in bloods with sub-clinical hypothyroidism

A

raised TSH
normal T3 and T4

151
Q

how to investigate thyroid nodules

A

US scan
fine needle aspiration

152
Q

what is euthyroid sick syndrome

A

systemic illness causing low T3/4 and TSH (rarely can be secondary hypothyroidism)

check if asymptomatic and if euthyroid clinically repeat TFTs one month later

153
Q

how to work out how many mg to give for levothyroxine

A

do 1.6 multiplied by their weight in kg

tablets come as 25mg so round to nearest 25

154
Q

levothyroxine and pregnancy

A

increase dose by 25-50mg (or 25%)

repeat TFTs every 4-6 weeks and titrate to TSH

refer to endocrinology for close monitoring of her antibodies- if raised need additional growth scans

155
Q

1st line management of T2D if they already have cardiovascular disease

A

metformin plus SGLT2 inhibitor

Semester 2 (3rd year) (12 decks)

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