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year 3 conditions > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

for which 2 groups of ppl is BMI inaccurate

A

pregnant
ppl with large amount of muscle mass

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2
Q

how to calculate BMI

A

kg / m^2

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3
Q

underweight BMI

A

<18.5

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4
Q

normal BMI

A

18.5 - 24.9

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5
Q

overweight BMI

A

25 - 29.9

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6
Q

obese BMI class 1 2 3

A

class 1
30 - 34.9

class 2
35 - 39.9

class 3
40+

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7
Q

management for class 1 obese

A

1st line = lifestyle modifications
consider orlistat

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8
Q

Mech of action of osrlistat

A

pancreatic lipase inhibitor

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9
Q

management of class 2 obesity with comormidities / class 3 obesity / other Tx been ineffective

A

bariatric surgery

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10
Q

which classes of obesity qualify for bariatric surgery

A

management of class 2 obesity with comormidities / class 3 obesity / other Tx been ineffective

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11
Q

2 roles of cobalamin / vit b12

A

rbc synthesis
myelination

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12
Q

where is b12 absorbed

A

terminal ileum

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13
Q

which foods is b12 found in

A

animal products

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14
Q

4 causes of b12 deficiency

A

pernicious anaemia
gastrectomy
vegan diet
disease of terminal ileum: crohns or ileocaecal resection

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15
Q

which cancer does pernicious anaemia increase risk of

A

gastric

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16
Q

what are the 2 types of antibodies that can be found in pernicious anaemia

A

anti - IF antibodies
anti gastric parietal cell antibodies

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17
Q

clinical features of vit b12 deficiency

A

anaemia (fatigue, pallor, SOB etc)
peripheral neuropathy (tingling, numbness etc)
dementia
glossitis

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18
Q

b 12 deficiency management

A

IM supplementation of vitamin B12 (hydroxocobalamin)

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19
Q

should you replace b12 or folate first

A

b12

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20
Q

describe the rbc’s in b12/folate deficiency

A

Macrocytic, Megaloblastic Anaemia
→ decreased Hb,
increased MCV,
hyperchromic RBCs,
hypersegmented neutrophils

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21
Q

describe homocysteine levels in b12 and folate deficiency

A

elevated in B12 & Folate deficiency

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22
Q

describe Methylmalonic acid (MMA) levels in B12 and folate deficiency

A

elevated in B12 deficiency,
normal in folate deficiency

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23
Q

2 roles of folate

A

DNA synthesis and amino acid metabolism

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24
Q

which vitamin is folate

A

vit B9

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25
Q

which food is folate found in

A

green leafy veg

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26
Q

4 causes of folate deficiency

A

malabsorption (small bowel disease due to IBD or coeliac disease),
malnutrition (chronic alcohol use),
increased requirement (pregnancy),
drug related (methotrexate, antiepileptics)

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27
Q

clinical features of folate deficiency

A

anaemia
glossitis
fetal spinal bifida if mother is deficinet

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28
Q

what does the foetus get if the mother is folate deficient

A

fetal spinal bifida
anacephaly

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29
Q

main difference in clinical features between vit b12 and folate deficiency

A

folate deficiency does not result in neurological symptoms

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30
Q

Tx for folate deficiency

A

oral folate supplementation

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31
Q

how much folate should pregnant women take to prevent fetal neural tube defects

A

400mcg of folic acid until the 12th week of pregnancy

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32
Q

definition of hypothermia

A

< 35

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33
Q

definition of hyperthermia

A

> 40

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34
Q

what is mild hypothermia

A

35 - 32

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35
Q

features of mild hypothermia

A

tachycardia, tachypnoea, shivering, vasoconstriction

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36
Q

what is moderate hypothermia

A

28 - 32

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37
Q

features of moderate hypothermia

A

arrhythmias, hypotension, resp depression, cognitive impairment, may cease to shiver

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38
Q

what is severe hypothermia

A

< 28

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39
Q

features of severe hypothermia

A

loss of/reduced consciousness
coma
arrhythmia
apnoea
fixed dilated pupils

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40
Q

which temp do you measure for hypothermia

A

core body temp

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41
Q

ECG hypothermia features

A

J / Osborn waves
broad QRS complex

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42
Q

mild hypothermia management

A

passive external rewarming (remove wet clothing, cover with blankets, warm room)

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43
Q

moderate hypothermia management

A

active external rewarming (warm blankets, radiant head, forced warm air)

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44
Q

severe hypothermia management

A

IV warmed crystalloid

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45
Q

hypothermia complications

A

arrhythmias
hypoglycaemia
hyperkalaemia
GI disorders
rhabdomyolysis

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46
Q

which temp do you measure for hyperthermia

A

rectal temp

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47
Q

heat stroke vs heat exhaustion

A

heat stroke = hyperthermia with CNS dysfunction
heat exhaustion = hyperthermia without CNS dysfunction

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48
Q

what are the 2 types of heat stroke

A

classic (due to external environment)
exertional

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49
Q

heat stroke symptoms

A

confusion
seizures
loss of consciousness
delirium

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50
Q

heat stroke management

A

stabilisation (ABC, remove clothes)
rapid active cooling (full body immersion in ice water)

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51
Q

heat exhaustion symptoms

A

nausea
dizziness
weakness
muscle cramps
fatigue
headache

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52
Q

heat exhaustion management

A

oral isotonic fluids
active cooling

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53
Q

which LDL and HDL levels promote atherosclerosis

A

Elevated LDL and reduced HDL

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54
Q

familial hypercholestrolaemia inheritance pattern and mutation

A

Autosomal dominant inherited disorder
Caused by a mutation in the gene coding the LDL receptor

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55
Q

clinical features of hyperlipidaemia

A

Xanthomata → nodular lipid deposits in the skin and tendons

Xanthelasma → yellow, flat plaques on upper eyelids
(xanthelasma is a type of xanthomata)

Corneal Arcus → crescentic-shaped opacity at the periphery of the corne

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56
Q

Ix for hyperlipidaamia

A

Lipid Profile → total cholesterol, HDL, LDL and trigylcerides

Tests for Secondary Causes → HbA1c/Fasting glucose, TSH, LFTs, urinalysis, LFTs

QRISK2 → screens for risk of cardiovascular disease.

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57
Q

QRISK < 10% management for hyperlipidaemia

A

lifestyle modifications

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58
Q

QRISK >= 10% management for hyperlipidaemia

A

atorvastatin 20mg
or simvastatin

or if they have IHD/PAD/cerebrovascular disease give atorvastatin 80mg

or if statin intolerant:
ezetimibe

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59
Q

in which pts is atorvastatin C/I

A

pregnant

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60
Q

Mech of action of ezetimibe

A

cholesterol absorption inhibitor

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61
Q

when should statins be taken to be most effective

A

last thing at night

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62
Q

when should statins be discontinued

A

if serum transaminase concentrations rise to and persist at 3 times the upper limit of the reference range

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63
Q

what is an important drug interaction of statins

A

with erythromycin/clarithromycin (macrolides) (can cause myopathy, increased likelihood of rhabdomyolysis)

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64
Q

which medication can cause both hypo and hyperthyroidism

A

amiodarone

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65
Q

list some side effects of amiodarone

A

hypothyroidism
hyperthyroidism
corneal deposits
Steven Johnsons syndrome
grey discolouration of the skin
liver failure
pneumonitis + pulmonary fibrosis

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66
Q

what type of medicine is aledronic acid

A

bisphosphonate

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67
Q

in which disease should bisphosphonates be avoided

A

advanced kidney disease

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68
Q

side effects of bisphosphonates

A

severe reflux disease
peptic ulceration
jaw necrosis

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69
Q

what med should be started in women with osteoperosis confirmed by DEXA scan or over 75yrs with 2+ risk factors for fracture / have had a previous fragility fracture

A

bisphosphonates eg aledronic acid

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70
Q

which side effect can spironolactone cause in men

A

gynaecomastia

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71
Q
A
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72
Q

symmetrical aches and pains
proximal muscle weakness
bone wearing fracture
waddling gait
likely diagnosis

A

osteomalacia

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73
Q

4 causes of osteomalacia

A

insufficient dietary calcium
vit D deficiency due to poor UV light exposure
CKD (causes low vit D which can cause low calcium)
malabsorption

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74
Q

what is osteopetrosis

A

defect in osteoclasts which means they cannot break down bone
results in denser bones and thickened bone cortices –> brittle bones
have stunted growth, bone pain, and bright hyper dense bones on imagining

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75
Q

joint and bone pain
stunted growth
in a child
likely diagnosis

A

rickets (childhood vit D deficiency)

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76
Q

bone pain
fractures
nausea
vomiting
constipation
high calcium, high PTH and ALP, low phosphate
likely diagnosis

A

hyperparathyroidism causing osteitis fibrosa csytica (excessive PTCH activates osteoclasts leading to increased bone resorption

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77
Q

weak deformed hyper vascular bones
normal calcium / phosphate / PTH
increased ALP
bone pain
symptoms in one bone only
likely diagnosis

A

pagets disease
–> is caused by deformed bone remodelling

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78
Q

MEN I symptoms

A

Parathyroid hyperplasia / adenoma
pituitary prolactinoma or GH secreting tumour (acromegaly)
Pancreas endocrine tumour (insulinoma, gastrinoma)

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79
Q

MEN IIa symptoms

A

thyroid cancer
parathyroid hyperplasia
bening and bilateral phaechromocytoma

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80
Q

MEN II b symptoms

A

Phaechromocytoma
Medullary thyroid cancer
mucosal neuroma
marfanoid appearance

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81
Q

tall stature
hypogonadism
gynaecomastia delayed puberty
likely diagnosis

A

Klinefelter’s syndrome (47 XXY)

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82
Q

what is the Rotterdam criteria for PCOS

A

2/3 of the below are needed for a diagnosis to be made
- presence of multiple ovarian cysts
- oligomenorrhoea or amnehorrhoea
- clinical/biochemical signs of hyperandrogenismeg acne/hirsutism/alopecia

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83
Q

oligomenhorroea
amenhorrea
galactorrrhoea
decreased libido
infertility
decreased bone mass
likely diagnosis

A

hyperprolcatinaemia

decsreased bone mass is due to decreases in oestrogen (hypogonadism)

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84
Q

oligomenhorrea
infertility
hirsutism
ambiguous genitalia
salt losing addisonian crisis

A

late onset congenital adrenal hyperplasia
(21 hydroxylate deficiency so can’t make cortisol and aldosterone, so make lots of androgens - high testosterone)

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85
Q

what diagnosis does recurrent chest infections and azoospermia point to

A

CF
(azoospermia is due to genesis of the vas deferens)

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86
Q

what effects does amiodarone withdrawal have on the thyroid

A

thyrotoxicosis

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87
Q

most common cause of hypopituitarism

A

pituitary adenoma

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88
Q

1st line investigation to confirm Addisons

A

measure cortisol.
if its low then do a short synthacten test - synthacten should stimulate cortisol production form the adrenal glands, this will not happen in Addisons

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89
Q

does parathyroid adenoma cause visible neck swelling

A

no

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90
Q

what is measured in the screening tests for medullary thyroid carcinoma

A

serum calcitonin

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91
Q

what is the effect of reduced Gh and gonadotrophin secretion on the bones

A

osteoporosis

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92
Q

1st line and definitive treatment for phaechromocytoma

A

alpha blockers eg Phenoxybenzamine

(then can add beta blocker to manage tachycardia/arrhythmias caused by alpha blockers, if needed)

then would do a phaechromocytoma resection (definitive management)

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93
Q

main side effect of phenoxybenzamine

A

reflex tachycardia

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94
Q
A
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95
Q

what is Waterhouse friderishcen syndrome (WS)

A

a severe, often fatal, disorder characterized by adrenal hemorrhage and failure, resulting from disseminated intravascular coagulation (DIC) triggered by a bacterial infection

presents initially with a nonspecific infection progressing into a macular, petechial, and subsequently purpuric rash, along with septic shock

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96
Q

most common cause of Waterhouse friderishcen syndrome (WS)

A

Neisseria meningitides
strep pneumonia

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97
Q

first line diagnostic test for phaechromocytoma

A

plasma free metenephrines

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98
Q

pt had cushings then had a bilateral adrenalectomy to treat it
they start to develop headaches and visual field defects

A

Nelsons syndrome
–> bilateral adrenalectomy causes loss of feedback to brain
therefore increased CRH release form hypothalamus
increased stimulation of pituitary causes enlargement and formation of pituitary adenoma

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99
Q

what is sick euthyroid syndrome

A

commonly seen during a period of illness
deranged low thyroid function tests despite normal functioning thyroid
will recover as the illness improves

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100
Q

which medications can cause a rise in prolactin levels

A

SSRI
cimetidine
BBs

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100
Q

how to manage galactorrhoea due to a certain drug, where the pt can’t stop taking the drug

A

co prescribe a dopamine agonist eg cabergoline to counteract the side effect - but manage with care bc cabergoline may reduce the effectiveness of the medication that they’re on

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101
Q

how to manage post partum thyroiditis

A

watch and wait
–> post part thyroiditis consists of hyperthyroidism then hypothyroidism. so if you give an antithyroid medication and then they become hypothyroid anyway, you could worsen things

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102
Q

what is made in each layer of the adrenal gland

A

Going deeper:
zona glomerulosa: aldosterone (salt)
zona fasciculata: glucocorticoids, cortisol (sugar)
zona reticularis: androgens (sex)

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103
Q

what medication is bromocriptine

A

dopamine agonist

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104
Q

what is li-fraumeni syndrome

A

a hereditary cancer predisposition syndrome associated with cancers such as leukaemia and sarcoma

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105
Q

first step in investigation/management of a pt with signs of cushings who is on long term steroid therapy currently

A

wean their steroid use
—> he first step would NOT be high/low dexamethasone suppression tests in this case as they would provide us with no further info, since she’s already on steroids and has high cortisol

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106
Q

treatment of subacute thyroiditis aka de quervains thyroiditis

A

supportive care and pain relief if needed (the condition will go from thyrotoxicosis, to hypothyroidism to euthryoidism)
antithyroid drugs dont work bc the thyrotoxicosis is due ti release of reframed hormones from the thyroid gland

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107
Q

at what age are boys with no pubertal development classed as having delayed puberty

A

14

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108
Q

which gene is associated with MEN 2a

A

RET gene

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109
Q

acute thyroiditis vs subacute thyroiditis

A

acute aka suppurative thyroiditis = caused by bacterial infection
presents with fever
presents quicker than subacute
rare

subacute thyroiditis aka de quervians = caused by viral infection
presents with painful neck, malaise
more common

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110
Q

initial screening test and result fro conns syndrome (primary hyperaldosteronism)

A

aldosterone to renin ratio
- elevated aldosterone causes sodium and therefore water retention. this increases renal perfusion, so inhibits renin secretion
high aldosterone, low renin
= high aldosterone: renin ratio

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111
Q

what is the aldosterone: renin ratio in primary vs secondary hyperaldosteronsim

A

high in primary eg conns syndrome
low in secondary - bc the aldosterone is elevated bc of the renin itself being elevated

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112
Q

best initial investigation in a young pt with poorly controlled HTN and hypokalaemia

A

aldosterone: renin ratio –> check for conns syndrome

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113
Q

what is the gold standard “challenge” test which is used ti clarify the diagnosis of hypopituitarism

A

insulin tolerance test
- stimulates hypoglycaemia wich aggravates a stress respinse

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114
Q

how does PTH act on bone to increase serum calcium levels

A

binds to osteoblasts which stimulate osteoclasts via porcine signalling

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115
Q

phaechromocytoma symptoms

A

episodic hypertension
palpitations
sweating

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116
Q

which hormones does a phaechromocytoma produce

A

it is a catecholamine producing tumour

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117
Q

potassium levels in conns syndrome vs Addisons

A

conns = hypokalaemia
Addisons = hyperkalaemia

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118
Q

which conditions are anti TPO antibodies found in

A

hashimotos or graves

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119
Q

how does PTh affect intestinal absorption of calcium and phosphate

A

increases intestinal absorption of both

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120
Q

carbimazole mech of action

A

inhibits TPO

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121
Q

palpitations, sweating, malignant hypertension
likely diagnosis

A

phaechromocytoma

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122
Q

which condition results in 2 or more specific neruoendocrine tumours (medullary thyroid cancer, phaechromocytoma, adenoma, parathyroid hyperplasia)

A

MEN 2a

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123
Q

what kind stature do MEN 2b sufferers have

A

marfanoid stature

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124
Q

what is the most likely cause of hyperprolactinamyia in young females with mental health problems

A

anti psychotics eg rsiperidone, tricyclic antidepressants, SSRIs, haloperidol

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125
Q

first line diagnosis test for cushings

A

overnight dexamethasone suppression test

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126
Q

first line investigation for delayed puberty

A

measure FSH and LH levels

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127
Q

what type of hypogonadism does kleinfleter’s cause

A

primary hypogonadism

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128
Q

what type of hypogonadism does kallman’s cause

A

secondary hypogonadism

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129
Q

what type of hypogonadism does cryptorchidism cause

A

primary hypogonadism

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130
Q

high TSH, normal T4
diagnosis

A

subclinical hypothyroidism

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131
Q

in what type of hyperaldosteronism are both renin and aldosterone raised

A

secondary hyperaldosteronism

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132
Q

causes of secondary hyperaldosteronism

A

nephrotic syndrome
liver cirrhosis
congestive heart failure
renal artery stenosis

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133
Q

young pt with high bp, sweating, headaches and anxiety
diagnosis

A

phaechormocytoma

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134
Q

an asymptomatic thyroid mass which is gradually getting larger in elderly pt
diagnosis

A

thryroid cyst / colloid nodule

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135
Q

what is involved on MEN1, MEN2a and MEN2b

A

MEN 1- (3 P’s) pancreas, parathyroid, pituitary
MEN 2A - (1M, 2P’s) Medullary thyroid cancer, pheochromocytoma, parathyroid
MEN 2B - (3M’s, 1P) Medullary thyroid cancer, Marfanoid, pheochromocytoma, mucosal neuroma

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136
Q

first line Tx for hypogonadism in men

A

testosterone therapy

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137
Q

first line investigation for hyperaldosteronism

A

aldosterone: renin ratio
(will be high in hyperaldosteronism)

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138
Q

gold standard for locating source of excess aldosterone in hyperaldosteronism

A

Selective adrenal venous sampling

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139
Q

treatment for hyperaldosteronism caused by bilateral adrenal disease

A

aldosterone antagonsists (Spironolactone, Eplerenone)

Then surgical resection

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140
Q

likely diagnosis for polyuria / polydipsia / headaches with osteoporosis

A

hyperaldosteronism

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141
Q

what is a well known heart complication of hyperthyroidism

A

atrial fibrillation

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142
Q

which condition is RET gene mutation associated with

A

MEN 2

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143
Q

male secondary sexual characteristics

A

the growth of pubic hair, and facial hair and the voice deepens

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144
Q

female secondary sexual characteristics

A

breasts develop, hips widen, and pubic hair begins to grow

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145
Q

long boy with small testicles, delayed puberty, gynaecomastia and no secondary sexual characteristics
likely diagnosis

A

kleinfelters

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146
Q

common cause of tingling after thyroid surgery

A

hypocalacemia - surgery may have affected the parathyroid glands

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147
Q

best investigation when looking for the cause of diabetes insipidus

A

MRI brain
(DI could be due to pituitary adenoma which is causing suppression of ADH secretion)

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148
Q

what is a neck lump which moves on swelling but not tongue protrusion suggestive of

A

a thyroid mass

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149
Q

most common cause of thyrotoxicosis in younger vs older pts

A

younger = graves
older = toxic multi nodular goitre

150
Q

describe the thyroid and associated symptoms of subclinical ( de quervians) thyroiditis

A

thyroid is small and tender to palpation
pt recently experinced infectious symptoms
pt is initially hyperthyroid, then euthyroid, then hypothyroid, then euthyroid again

151
Q

carbimazole mech of action

A

inhibits TPO

152
Q

what is Waterhouse-Friderichsen’s syndrome

A

adrenal haemorrhage and consequent adrenal failure

153
Q

if cortisol is high after overdose dexamethasone suppression test but is suppressed after high dose dexamethasone suppression test, which investigation needs to be conducted next

A

MRI of pituitary
- if they respond to his dose dexamethasone suppression test, its cusihings disease (due to pituitary adenoma), if they dont respond its ectopic ACTH production

154
Q

give examples of potassium sparing diuretics

A

sprionolcatone
amiloride
Eplerenone
Triamterene

155
Q

what type of diuretic is furosemide

A

loop diuretic

156
Q

which medication is given to someone with hypertension, hypokalaemia and bilateral adrenal disease

A

potassium sparing diuretic
eg sprionolcatone
amiloride
Eplerenone
Triamterene

157
Q

what kind of goitre would a non functioning adenoma cause

A

nodular goitre

158
Q

what is the main complication of any decrease in FSH/LH and oestrogen/testosterone

A

osteoporosis

159
Q

which scan is used to detect oestoperosis

A

DEXA scan

160
Q

what is Waterhouse friderichsen syndrome

A

adrenal gland failure due to bleeding in the adrenal gland, usually caused by severe meningitis or bacterial infection

161
Q

likely diagnose: pot and meningitis then developed persistently low glucose levels and increased skin pigmentation

A

Waterhouse friderichsen syndrome

162
Q
A
162
Q

what advice should be given with regards to steroids and intercurrent illness

A

double steroid dose

163
Q

which features make graves eye disease be classed as more severe

A

lid retraction > 2mm
significant soft tissue involvement
exophthalmos > 3mm
diplopia
optic neuropathy
corneal breakdown

164
Q

what does tds mean

A

three times a day

165
Q

what does bd mean

A

twice a day

166
Q

what does qid mean

A

4 times a day

167
Q

which antithyroid drugs cause agranulocytosis

A

PTU
carbimazole
methimazole

168
Q

what kind of hyperaldosteronism does a renin producing tumour cause

A

secondly hyperaldsteronism

169
Q

what sort of ph class does conns syndrome cause

A

metabolic alkalosis (bc it increases urinary acidification)

170
Q

which cancers most comply release ectopic ACTH

A

small cell lung cancer
carcinoid tumours

171
Q

which cause of hyperthyroidism would present with reduced uptake on a radioisotope scan

A

de quervain’s thyroiditis

172
Q

which cause of hyperthyroidism would present with diffuse uptake on a radioisotope scan

A

graves

173
Q

which cause of hyperthyroidism would present with patchy uptake on a radioisotope scan

A

toxic multi nodular goitre

174
Q

which cause of hyperthyroidism would present with uptake in only one area on a radioisotope scan

A

toxic thyroid adenoma

175
Q

whats the difference between hot and cold nodules on an iodine 123 thyroid scan

A

hot = functional eg causes hyperthyroidism
cold = non functional - malignant

176
Q

best investigation to do for pt with a thyroid mass who has abnormal TSH and T3/4

A

fine needle aspiration- could be a malignancy

177
Q

which thyroid cancer has the worst prognosis

A

anapaestic thyroid cancer - most case lead to rapid death

178
Q

where does a medullary thyroid cancer metastasis to

A

lymph nodes, liver, bones, and lungs

179
Q

which cause of hyperthyroidism classically presents as a painful smooth goitre

A

de quervain’s thyroiditis

180
Q

which cause of hyperthyroidism classically presents as a painful nodular goitre

A

toxic solitary adenoma

181
Q

which cause of hyperthyroidism classically presents as a painless smooth goitre

A

graves

182
Q

someone who is usually on long term steroids collapses and is found to have hyponatraemia, hypokalaemia and hypoglycaemia - likely diagnosis

A

adrenal crisis

183
Q

likely diagnosis: high cortisol in low dose dexamethasone suppression test
high cortisol and low ACTH in high dose dexamethasone suppression test

A

adrenal adenoma

184
Q

likely diagnosis: high cortisol in low dose dexamethasone suppression test
high cortisol and high ACTH in high dose dexamethasone suppression test

A

topic source of ACTH (eg small cell lung cancer or carcinoid tumour)

185
Q

likely diagnosis: high cortisol in low dose dexamethasone suppression test
low cortisol and low ACTH in high dose dexamethasone suppression test

A

cushings disease

186
Q

medication prescribed in post partum thyroiditis

A

propanolol
- just like with de quervain’s thyroiditis, the hyperthyroidism is transient, so you down give anti thyroid drugs, just symptomatic relief

187
Q

Tx for tertiary hyperparathyroidism

A

parathyroidectomy

188
Q

which is the most common antibody in graves

A

TSHr antibodies
(anti TPO antibodies are also present but are less common)

189
Q

aldosterone mech of action on nephron

A

increases Na reabsorption into blood
increases K and H+ secretion into urine

190
Q

what does a high aldosterone: renin ratio indicate

A

conns syndrome

191
Q

[t has low calcium, high phosphate and short 4/5th metacarpal
diagnosis?

A

pseudohypopituitarism (autosomal dominant contain, reisstance to PTH)

192
Q

which T3/4 and TSH pattern would a poor compliance with levothyroxine show

A

normal T3/4
raised TSH
(T4 replacement has been intermittent so has been unable to suppress the TSH)

193
Q

which type of thyroid cancer is the most rapidly and aggressively growing and invades local structures

A

anaplastic thyroid cancer

194
Q

pt presents with thyroid mass that has appeared 2 weeks ago and has been rapidly growing, they also have some cervical lymphadenopathy
likely diaganosis?

A

anaplastic thyroid cancer

195
Q

first investigation and confirmatory investigation do to if suspect primary hyperaldosteronism

A

aldosterone: renin ratio first (high ratio is suggestive)
then fludrocortisone suppression test to confirm- fludrocortisone ownt suppress aldosterone production in primary hyperaldosteronism

196
Q

4 causes of primary hyperaldosteronism

A

Adrenal adenoma (Conn’s Syndrome): Often associated with primary hyperaldosteronism.
Bilateral adrenal hyperplasia: Common cause of Conn’s Syndrome.
Familial hyperaldosteronism: Rare genetic conditions leading to excessive aldosterone production.
Adrenal carcinoma: A rare malignant growth within the adrenal gland

197
Q

which blood test should e done if you are worried a pt on carbimazole has developed sepsis due to agranulocytosis

A

FBC and blood culture

198
Q

what levels of calcium and PTH would be seen in malignant hyperparathyroidism

A

high calcium with low parathyroid hormone (as parathyroid hormone-related protein mimics parathyroid hormone but is not detected in the assay)

199
Q

what is myxoedema crisis a complication of

A

untreated hypothryoidism

200
Q

history of visual problems
sudden onset retro orbital headache
nausea / vomiting
likely diagnosis

A

pituitary apoplexy
(a rare emergency and is defined as bleeding into the pituitary gland that occurs in patients who have pituitary tumours)

201
Q

patients >50 years old associated with a raised ESR, jaw and tongue claudication and visual change
temporal artery thickening , loss of pulsation and tenderness and may have proximal stiffness
likely diagnosis

A

giant cell arteritis

202
Q

what medication should be prescribe to treat vit D deficiency

A

ergocalciferol

203
Q

what are the 4Ds of vitamin B3 (niacin) deficiency

A

diarrhoea
dermatitis - brown scaly rash on hands and neck (Casal necklace)
dementia
death

204
Q

vegetarian starts to experience reduced sensation and pins and needles
which vitamin is she likely to be deficient in

A

B12
(vitamin B12 comes from animal products such as meat, fish and eggs. Vitamin B12 deficiency causes neurological symptoms, including peripheral neuropathy, visual changes and cognitive changes)

205
Q

deficiency of which vitamin are white spots (“bitot’s spots”) on the conjunctiva suggestive of

A

vit A

206
Q

what should be checked before a pt is started on levothyroxine

A

serum cortisol level
This is because patients with primary hypothyroidism may have additional autoimmune conditions such as hypoadrenalism and replacement of thyroid hormones may precipitate an adrenal crisis.

207
Q

child with DKA complains of headache, has a deterioration in neurological status and bradycardia. what condition should be urgently checked for

A

cerebral oedema (swelling of brain parenchyma)

208
Q

ABs for hashimotos

A

anti TPO ab

209
Q

UK guidlines for diagnosing DKA

A

blood ketone levels ≥ 3.0 mmol/L

hyperglycaemia
(blood glucose > 11.0 mmol/L)

acidosis
(bicarbonate < 15.0 mmol/L and/or venous pH < 7.3).

210
Q

projectile non-bile-stained vomiting following feeds, usually within the first 6 weeks of life and rarely in older children

diagnosis?

A

pyloric stenosis

211
Q

what is the effect of calcium carbonate on levothyroxine

A

Calcium carbonate decreases the absorption of oral Levothyroxine. They should be taken 4 hours apart

212
Q

what is diabetic ketosis

A

Hyperglycaemia and raised ketones in the absence of acidosis

213
Q

which antibodies are seen in post partum thryoditis

A

anti TPO antibodies

214
Q

which quick investigations can one done to assess for DKA

A

capillary blood gas (quicker, less distressing and just as beneficial as ABG)
capillary blood ketones

215
Q

what VBG result does diarrhoea cause

A

Normal Anion Gap Metabolic Acidosis.

216
Q

what VBG result does hypokalaemia cause

A

Metabolic alkalosis

217
Q

what VBG result does Addisons disease cause

A

Normal Anion Gap Metabolic Acidosis

218
Q

what VBG does vomiting cause

A

metabolic alkalosis

219
Q

a cause of raised anion gap (>16) metabolic acidosis

A

diabetic ketoacidosis

220
Q

what is the DVLA guidance surrounding hypoglycaemia

A

if a patient has more than one severe episode of hypoglycaemia whilst awake or one episode of severe hypoglycaemia (ie the pt required help from another person to mange it) whilst driving then they must stop driving immediately and inform the DVLA

221
Q

what is hypoglycaemic unawareness

A

patient is having a hypoglycaemic attack but does not show the normal symptoms of hypoglycaemia such as shaking, sweating, tremor

222
Q

how to treat hypoglycaemic attack in a pt with hypoglycaemic unawareness

A

glucogel

223
Q

levothyroxine dose for over 65 / adults with history of CVD

A

25-50 ug

224
Q

best first line Ix for pt presenting with hair loss

A

Thyroid function tests and ferritin

225
Q

diagnosis if a pregnant women presents with normal TSH but low t3/t4

A

normal physiology - Low free T3 and T4 levels in the second and third trimester of pregnancy is normal

226
Q

what is pandered syndrome

A

an inherited disorder where there is a defect in thyroxine synthesis leading to hypothyroidism. This tends to present at an early age

227
Q

most likely cause of deterioration a few hours into treatment for DKA

A

cerebral oedema

228
Q

best test for differentiating an endogenous from an exogenous cause of hypoglycaemia

A

Serum C peptide

Serum C-peptide is a byproduct of insulin production. Therefore, if it is raised this indicates that there is excessive endogenous insulin production. In contrast, if it is not raised then this indicates that the patient has administered herself insulin

229
Q

most common cause of hypothyroidism with negative antibodies

A

iodine deficiency

230
Q

which parts of the world have high prevalence of iodine deficiency

A

Middle East, Nepal (for the purposes of exams) and parts of South America

231
Q

how long should a dehydrated child with DKA (but not in shock) be given 10ml/kg 0.9% NaCl fluids for

A

30 mins

232
Q

which anti hyperglycaemic drug is most likely to cause a hypoglycaemic event

A

sulphonylureas eg gliclazdie

233
Q

difficulty concentrating, hair loss and joint pain, heavy menstrual periods
likely diagnosis?

A

hypothyroidism

234
Q

effect of hypothyroidism on periods

A

causes heavy menstrual periods

235
Q

effect of hyperthyroidism on periods

A

irregular, lighter or missed periods

236
Q

if a patient is unconscious with hypoglycaemia in a hospital ward, do you give IM glucagon or IV dextrose

A

IV dextrose (10%)
this is a more rapid way of treating hypoglycaemia and the pt is likely to have IV access as its in the hospital
IM glucagon is suitable in treating hypoglycaemia, but it has a slower duration of action (hours instead of minutes). Therefore, IM glucagon is preferred only when IV access cannot be established.

237
Q

what is losing the lateral third of eyebrow suggestive of

A

hair loss due to possible hypothyroidism

238
Q

diagnostic test for insulinoma

A

72 hr fast
A 72 hour supervised fast is key to observing a monitored drop in blood glucose levels and then at the moment of proper hypoglycaemia taking the correct hormonal blood profile which would include plasma insulin levels, pre-insulin, pre-pro insulin and ketones amongst others

239
Q

which drugs can affect the absorption of levothyroxine

A

ferrous sulphate
calcium chloride,
digoxin
Hormone Replacement Therapy

240
Q

side effect of levothyroxine

A

osteoporosis

241
Q

contrast the mechanism and causes of CDI and NDI

A

Central DI (More common)
insufficient levels of ADH from posterior pituitary.
Causes:
pituitary tumour/surgery,
traumatic brain injury,
infection (meningitis),
sarcoidosis,
TB,
SAH,
hereditary haemochromatosis

Nephrogenic DI
defective ADH receptors in the distal tubules and collecting ducts.
Causes:
lithium therapy,
electrolyte imbalances (hypercalcaemia or hypokalaemia),
idiopathic,
inherited (AVP2 gene)

242
Q

which receptors in the collecting duct does ADH work on

A

increases water reabsorption into blood in collecting duct via V2 receptors

243
Q

symptoms of DI

A

polyuria with very DILUTE URINE
nocturia
polydipsia
dehydration
no symptoms suggestive of DM

244
Q

what is the urine and plasma osmolality in DI

A

Low urine osmolality + High serum osmolality

245
Q

contrast plasma/urine osmolality and sodium levels in DI and psychogenic polydipsia

A

DI:
low urine osmolality
high plasma osmolality
hypernatraemia (and hypokalaemia)

PP:
low urine osmolality
high plasma osmolality
hyponatraemia

246
Q

glucose levels in DI

A

normal

247
Q

sodium and potassium conc in DI

A

high sodium conc
low potassium conc

(bc dehydrated)

248
Q

which test can be used to differentiate PP, CDI and NDI

A

1) low plasma osmolality, low urine osmolality –> PP
high plasma osmolality, low urine osmolality –> DI

2) do water deprivation test
If osmolality corrects itself then more sure it’s psychogenic polydipsia

3) If no correction, after 8 hours administer desmopressin to differentiate between CDI and NDI.

4)Urine osmolality will rise in CDI but remain low in NDI.

249
Q

how to mange hypernatraemia in DI, and what should you be cautious about

A

manage with oral or IV fluids (prevent dehydration)

(be careful, as correction of chronic hypernatraemia too fast predisposes to cerebral oedema)

250
Q

CDI Tx

A

intranasal desmopressin

251
Q

NDI Tx

A

discontinue causative agent if medication induced (lithium),
Thiazide Diuretics,
sodium restriction

252
Q

whipple’s triad for hypoglycaemia

A

low blood glucose concentration,
hypoglycaemic symptoms
resolution of symptoms after raising blood glucose concentration to normal

253
Q

causes of hypoglycaemia in diabetics

A

insulin or sulfonylurea use,
fasting/missing meals

254
Q

drugs which cause hypoglycaemia

A

sulfonylureas and insulin,
SGLT-2 inhibitors,
DPP-4 inhibitors

255
Q

hormone deficient which cause hypoglycaemia

A

hypopituitarism
adrenal insufficiency (Addisons)

256
Q

malignant cause fo hypoglycaemia

A

Insulinoma (excessive secretion of insulin due to tumour in pancreas)

257
Q

3 categories of symptoms in hypoglycaemia

A
  • Increased Sympathetic Activity
    sweating, anxiety, tachycardia, tremor, palpitations, pallor
  • Increased Parasympathetic Activity
    hunger, nausea, vomiting, paraesthesia
  • Neuroglycopenic
    confusion, seizures, agitation
258
Q

which glucose levels cause neuroglycopenic symptoms and autonomic symptoms in hypoglycaemia

A

<2.8 mmol/L causes neuroglycopenic symptoms,

<3.3 mmol/L causes autonomic symptom

259
Q

what can be measured to determine whether hypoglycaemia is due to endogenous or exogenous insulin

A

C peptide - high C peptide = endogenous insulin eg insulinoma

260
Q

what is the cause of hypoglycaemia if C peptide and insulin are high

A

insulinoma

261
Q

what is the cause of hypoglycaemia if cortisol is low

A

adrenal insufficiency (Addisons)

262
Q

what should you always measure in any patient presenting with confusion/neurological symptoms

A

measure blood glucose

263
Q

insulinoma Tx

A

surgical excision

264
Q

hypoglycaemia Tx in conscious pt who is able to swallow

A

oral glucose 15-20g (liquid, gel or tablet)
fast-acting carbohydrates (glucose tablets, candy, juice)

265
Q

hypoglycaemia Tx in unconscious pt

A

IM Glucagon (takes hours to work)
IV Dextrose (20% Glucose) (more rapid or if glucagon doesn’t improve symptoms)

if have access to IV, use Iv dextrose, if in community use IM glucagon in meantime

266
Q

describe the process of developing DKA

A

1)infection / inadequate insulin therapy / undiagnosed T1DM / MI

2)no insulin to suppress lipolysis

3) ketone formation

4) acidosis

267
Q

how could infection cause DKA and what are the sick day rules

A

Infection/illness
→ increased cortisol (antagonist of insulin)
→ bodies insulin requirements increase
⇒ hence type 1 diabetics should make sure they continue taking insulin when they are unwell to prevent DKA

‘Sick Day Rules’
⇒ continue normal insulin dose,
check blood glucose more regularly,
aim to drink 3L of fluid over 24hrs,
self-monitor ketones regularly through day.

268
Q

DKA symptoms

A

N&V
severe abdo pain
Kussmauls breathing - hyperventilation
Dehydration → dry mucous membranes, decreased skin turgor, slow CRT, tachycardic, hypotensive
reduced consciousness
fruity breath
rapid onset <24hrs

269
Q

VBG in DKA

A

metabolic acidiosis with raised anion gap (>16), with partial respiratory compensation (hyperventilation)

270
Q

glucose level in DKA

A

HIGH

271
Q

sodium and potassium in DKA

A

low sodium
high potassium

due to lack of insulin

272
Q

UK guidlines for DKA diagnosis

A

blood ketone levels ≥ 3.0 mmol/L
hyperglycaemia (blood glucose > 11.0 mmol/L)
acidosis (bicarbonate < 15.0 mmol/L and/or venous pH < 7.3

273
Q

what should be given in DKA if there is severe metabolic acidosis

A

IV bicarbonate

274
Q

how should regular insulin medication be adjusted after DKA

A

continue long acting insulin, stop short acting insulin

275
Q

2 key parts of DKA Tx

A
  1. Rehydrate → IV Fluids (Isotonic Saline - 10ml/kg 0.9% NaCl)

important complication of fluid resuscitation in DKA = cerebral oedema (may cause headache, reduced consciousness, rise in BP, seizures)

With Electrolyte repletion (especially K+ as insulin will drive it into cells) → Potassium Chloride

  1. Reduce Ketones → fixed rate IV Insulin (0.1 units/kg/hour) (AFTER FLUIDS)

Once glucose falls, give 5% dextrose

276
Q

in which people does HHS commonly occur

A

older people with T2DM

277
Q

why is DKA prevented in HHS

A

there is still smalll amounts of insulin being secreted by the pancreas

278
Q

RF for HHS

A

infection (most commonly pneumonia or UTI),
surgery,
inadequate insulin therapy,
acute illness(MI, sepsis, stroke),
non-adherence to diabetes medications

279
Q

what are the main components of HHS

A

hyperglycaemia (>30),
hyperosmolality (>320),
volume depletion (dehydration)
in the absence of significant ketoacidosis

280
Q

DKA vs HHS

A

both have
N&V,
features of dehydration,
weight loss/polyuria/polydipsia

DKA =rapid onset <24hs, HHS = more insidious onset over days

DKA = abdominal pain, HHS = no abo pain

DKA = fruity breath odour and kussmaul respirations)
^ not seen in HHS

DKA = normal serum osmolality, HHS = significantly risen serum osmolality

281
Q

ketones in HHS

A

negative

282
Q

what is the key parameter to monitor in HHS

A

serum osmolality - is significantly raised in HHS

283
Q

how to estimate serum osmolality in HHS

A

Estimated Serum Osmolality = 2(Na+K) + Glucose + Urea

284
Q

Tx for HHS

A

Fluid Resuscitation (IV Fluids) → Isotonic Saline solution (0.9% NaCl)

  • Excessive infusion of NaCl
    ⇒ can cause hyperchloraemic acidosis (hence hartmann’s solution may be preffered when large volumes of fluid are to be administered).
  • Excessive infusion of any IV fluid can cause pulmonary oedema and potentially cardiac failure.

Electrolyte Repletion (if needed) → add potassium (KCl) to infusion

  • IV Insulin (0.05 units/kg/hr)
    → not given first, as can result in cerebral oedema due to quick shift in glucose.
  • If Glucose falls
    → 5% Dextrose
285
Q

2 things to be cautious about during fluid resuscitation in HHS

A

excessive infusion of NaCl can cause hyperchloraemic acidosis - so can use Hartmanns solution when need to infuse a large volume

excessive infusion of any IV fluid can cause pulmonary / cerebral oedema and cardiac failure –> monitor for this (cerebral oedema will present as headache/pain, the deterioration)

286
Q

order of progression of the types of diabetic eye disease

A

Background Retinopathy → Pre-Proliferative Retinopathy → Proliferative Retinopathy (Also Maculopathy)

287
Q

which 2 things can cause complete loss of vision in diabetic eye disease

A

retinal detachment
vitreous haemorrhage

288
Q

retinal detachment vs vitreous haemorrhage

A

retinal detachment:
- sudden painless loss of bison
flashers
floaters
dense shadow starts peripherally and moves central

vitreous haemorrhage
- bleeding into nitrous humour
sudden blurring
dark spots
floaters
NO flashers

289
Q

fundoscopy findings in background / pre proliferative / proliferative retinopathy and maculopathy

A

○ Background → microaneurysms, blot haemorrhages, hard exudates (lipid deposits)

○ Pre-Proliferative → background + cotton wool spots (soft exudates)

○ Proliferative → non-proliverative + neovascularisation (new vessels on disk)

Maculopathy → hard exudates (ie. background retinopathy) that happens to be near macula

290
Q

background retinopathy Tx

A

improve glycaemic control and regular observation

291
Q

pre proliferative and proliferative retinopathy Tx

A

pan-retinal laser photocoagulation

292
Q

maculopathy Tx

A

VEGF inhibitors

293
Q

what is diabetic neuropathy caused by

A

blockage of vasa nervorum

294
Q

how does chronic hyperglycaemia cause diabetic neuropathy

A

causes glycation of axons

295
Q

features of diabetic neuropathy

A

MOSTLY AFFECTS SENSORY AXONS, BUT CAN AFFECT A SOME MOTOR AXONS TO A LESSER EXTENT

Peripheral Neuropathy:

* Pain (Peripheral) → described as burning/sticking/aching. Often worse at night and may disturb sleep.

* Loss of Sensation (Peripheral) → at early stage affects tips of toes or fingers. Eventually causes a symmetrical distal sensory loss in a 'glove and stocking distribution’.

* Dysaesthesia (Peripheral) → burning sensation in feet

* Reduced/Absent Ankle Reflexes (Peripheral)

* Painless Injuries (Peripheral) 
→ occur at pressure points. 
Infection is a common complication, followed by gangerene if vascular compromise.

Mononeuropathy
→ sudden motor loss (eg. wrist drop, foot drop, 3rd nerve palsy - down and out eye)

Autonomic
→ resting tachycardia,
urinary frequency/urgency/nocturia/incontinonence/hesitency/weak stream/retention,
erectile dysfunction,
constipation,
difficulty swallowing,
postural hypotension
Gastroparesis (GI Autonomic Neuropathy)

296
Q

what treatment should be initiated if someone with diabetic neuropathy begins to experience N&V, abdo pain, bloating, loss of appetite, refleux

A

metoclopramide
(Gastroparesis)

297
Q

mech of action of metoclopramide

A

pro-kinetic that improves gastric emptying

298
Q

Ix for diabetic neuropathy

A

Test sensation using 10g monofilament

Tuning fork (decreased vibration sense), Pinprick assessment (decreased sensation)

299
Q

where are neuropathic ulcers often seen in diabetic neuropathy

A

over pressure points eg
plantar surface of metatarsal head
plantar surface of hallux

300
Q

Tx for pain associated with diabetic neuropathy

A

1st line = duloxetine
2nd line = amitriptyline, gabapentin or pregabalin
Avoid amitriptyline in patients with BPH as can cause urinary retention

301
Q

which pts should amitriptyline be avoided in

A

Avoid amitriptyline in patients with BPH as can cause urinary retention

302
Q

3 major histological changes of diabetic nephropathy

A

mesangial expansion,
glomerular basement membrane thickening,
Glomerulosclerosis

303
Q

symptoms of diabetic nephropathy

A
  • Hypertension
  • Oedema → in advancing diabetic nephropathy
  • Polyuria
  • Lethargy
304
Q

first line Ix for diabetic nephropathy

A

urinalysis
(ACR >2.5 = microalbuminuria)

305
Q

how and how often should pts be screened for diabetic nephropathy

A

anual screening
using urinary ACR (ACR >2.5 = microalbuminuria)

306
Q

gold standard Ix for diabetic nephropathy

A
  • Gold Standard: Renal Biopsy
    → shows kimmelstiel-wilson nodules (also mesangial expansion and GBM thickening)
307
Q

eGFR level in diabetic nephropathy

A

GFR raised in early disease but reduced in late disease

308
Q

management of diabetic nephropathy

A

Antihypertensive Treatment
→ ACE inhibitors or ARBs are first line (renoprotective effect).
Add CCB or Thiazide Diuretic as 2nd line.

Tight Glycaemic Control

Control Dyslipidaemia
→ Statins (atorvastatin)

Dietary Modification
→ reduce protein and salt intake

Smoking Cessation

309
Q

what is seen on renal biopsy for diabetic nephropathy

A

kimmelstiel-wilson nodules

310
Q

which medication can cause diabetes

A

corticosteroids

311
Q

metformin side effects

A

lactic acidosis
Gi effects
- diarrhoea
- N&V
- abdo discomfort
Metallic taste in mouth

–> weight NEUTRAL

312
Q

what is recommended for pts with a fasting glucose of >5.6mmol/L but <7mmol/L

A

2 week trial fo diet and exercise

313
Q

which antidiabetic drugs can cause acidosis and whats the difference n the acidosis they cause

A

metformin. - lactic acidosis (NO KETONES)
SGLT2 inhibitor - ketoacidosis

314
Q

which anti HTN drugs are teratogenic

A

ACE inhibitors

315
Q

metformin mech of action

A

increases insulin sensitivity
reduces hepatic gluconeogenesis

316
Q

when can metformin be prescribed

A

if HbA1C ≥48 despite lifestyle advice

317
Q

which conditions are type 1 diabetes pts checked for due to the common association between them

A

autoimmune thyroid disease
coeliac disease
autoimmune gastrotis
pernicious anaemia
vitiligo

318
Q

criteria for diagnosing T2DM

A

If symptomatic, one of the following results is sufficient for diagnosis:

  • Random blood glucose ≥ 11.1mmol/l
  • 2-hour glucose tolerance ≥ 11.1mmol/l
  • HbA1C ≥ 48mmol/mol (6.5%)

If the patient is asymptomatic, two results are required from different days.

or
2 abnormal fasting glucose results
* Fasting plasma glucose ≥ 7mmol/l

319
Q

what type of drug is glimepiride

A

sulphonylurea

320
Q

which microorganism is commonly found in diabetic foot ulcers

A

Pseudomonas

321
Q

what is the honeymoon period in T1DM

A

Immediately after diagnosis, insulin requirements may be very low if the pancreas is still able to produce a significant amount of insulin. This is known as the ‘honeymoon period’. It is important that children are closely monitored during this time. This is because insulin requirements can suddenly increase as the remaining beta cells are destroyed. Additionally, as the blood glucose may be normal in this period on very low insulin doses, parents may incorrectly think that the condition has gone away.

322
Q

first lien Tx for T1DM

A

basal bolus insulin, or if pt has good self-management skills may prefer to use an Insulin pump

323
Q

which pts can receive fixed dose insulin

A

if they cannot manage 3-4 insulin injections daily, or have trouble mixing the insulin

324
Q

what should be the target bp for diabetic pts

A

140/90

325
Q

what counts as an impaired fasting glucose

A

6.1-6.9 mol/L

326
Q

what counts as a diabetic fasting glucose

A

7+ mmol/L

327
Q

what counts as impaired glucose tolerance (2hr OGTT)

A

7.8-11 mmol/L

328
Q

what counts as a diabetic glucose tolerance (2hr OGTT)

A

11.1+ mmol/L

329
Q

can C peptide levels be used to diagnose diabetes

A

no, can be used to differentiate between type 1 and 2 diabetes

330
Q

when can just a random blood glucose result be sued to diagnose diabetes

A

One measurement of blood glucose >11.1mmol/L in a symptomatic patient is sufficient to diagnose diabetes mellitus

331
Q

which anti diabetic medication can cause weight gain

A

sulphonylurea
(and pioglitazone)

332
Q

what is a high risk contributor to the development of gestational diabetes

A

maternal obesity (BMI>30)

333
Q

type 2 diabetic pt presents with hypoglycaemia, which medication could have caused this

A

sulphonylurea eg gliclazide

334
Q

what kind of diabetic drug is glibenclamide

A

sulpohonylurea

335
Q

what will pulses and foot temp be like in the case of an arterial leg ulcer vs neuropathic foot ulcer

A

palpable pulses and warm foot in neuropathic not arterial

336
Q

moat appropriate initial Ix for diabetic retinopathy

A

fundoscopy

337
Q

target HbA1c for diabetic pt managed by diet / lifestyle / single drug

A

48

338
Q

target HbA1c for diabetic pt managed by 2+ drugs / sulphonylurea

A

53

339
Q

T1DM diagnosis

A

If symptomatic, one of the following results is sufficient for diagnosis:

Random blood glucose ≥ 11.1mmol/l or Fasting plasma glucose ≥ 7mmol/l
2-hour glucose tolerance ≥ 11.1mmol/l
HbA1C ≥ 48mmol/mol (6.5%)
If the patient is asymptomatic, two results are required from different days.

To confirm T1DM, the following investigations can be done:
Autoantibody testing: Identification of specific antibodies (e.g. anti-GAD, ICA, IAA) contributes to confirming the autoimmune nature of T1DM.

C-peptide levels: Evaluation of C-peptide production helps assess endogenous insulin secretion.

Urine ketone testing: Presence of ketones may suggest concurrent DKA.

340
Q

best initial Ix for T1DM

A

glucose - faster and more accurate than HbA1c - takes longer and level can be affected by other things

341
Q

what type of medicine is indapamide

A

diuretic

342
Q

recommendation for pt taking metformin when fasting during ramadan

A

Continue on 500mg, take the morning dose before Suhoor (pre-sunrise meal), combine afternoon dose with dose taken at Iftar (after sunset meal)

343
Q

most common autoantibodies associated with T1DM

A

ICA (islet cell autoantibodies) —> MOST COMMON
anti GAD antibodies (glutamic acid decarboxylase)
IAA (insulin autoantibodies)

344
Q

what is balanitis

A

inflammation of glans penis

345
Q

what should be prescribed if a T2DM pt has symptomatic hyperglycaemia,ia

A

insulin or a sulphonylurea

346
Q

after starting medication for diabetes what should be checked at 3-6 monthly intervals

A

check HbA1c at 3-6 monthly intervals until it is stable on a set diabetes treatment plan.

347
Q

how often should diabetic retinopathy / nephropathy / neuropathy be screened for in diabetic pts

A

at diagnosis, and then annually

348
Q

what is allodynia

A

pain due to a stimulus that does not normally provoke pain.
An example would be a light feather touch (that should only produce sensation), causing pain.

349
Q

which condition presents with ascending cure bilateral motor loss

A

Guillain-barre (auto-immune condition against nerves)

350
Q

which ulcers are commonly found above the medial or lateral malleolus

A

venous ulcers

351
Q

first course of action in gastroparesis due to diabetic neuropathy

A

stabilise blood glucose levels

352
Q

what is listeriosis

A

serious infection caused by eating food contaminated with listeria bacteria eg cold cooked sliced meats

353
Q

normal / average birth weight

A

2.5 kg - 4kg

354
Q

what is AGPAR score and what is a normal score

A

test given to newborns a few minutes after birth - checks HR, muscle tone etc to check baby’s stability
normal = 7-10

355
Q

what is macrosomia

A

birth weight > 4kg

356
Q

what does macrosomia and neonatal seizures suggest

A

gestational diabetes in the mother

357
Q

how does pre eclampsia affect weight of babies

A

lower birth weight due to reduced placental blood flow

358
Q

what do neonatal seizures, microcephaly, petechial rash, jaundice and low birthweight suggest

A

CMV transmitted vertically from mother to foetus

359
Q

diagnostic criteria for gestational diabetes

A

either:
a fasting plasma glucose level of ≥5.6 mmol/L;
or
a 2-hour post-oral glucose tolerance test plasma glucose level of ≥7.8 mmol/L

360
Q

when would you use short/rapid acting subcutaneous insulin vs fixed rate insulin infusion

A

fixed rate insulin infusion: hyperglycaemic crisis eg HHS
rapid acting subcutaneous insulin: patient develops hyperglycaemia, has been present fro several hours and is not resolving, pt is not critically unwell

361
Q

which anti diabetic medications should be stopped when a pt is reaching the last phase of heir life

A

medications which can cause hypoglycaemia eg Sulphony;ureas

361
Q

risk of mother under 25 yrs w T1DM passing it onto child

A

1/25

362
Q

3 reasons for immediate referral to an ophthalmologist in the case of diabetic retinopathy

A

proliferative retinopathy - angiogenesis / neovascularisation
vitreous haemorrhage
retinal detachment

363
Q

urine osmolality after fluid deprivation n and after desmopressin in partial cranial DI

A

A urine osmolality of 300-800mOsm/kg after fluid deprivation
and
<800mOsm/kg after desmopressin

364
Q

which cells produce insulin

A

beta cells

365
Q

how can bendroflumethiazide cause elevated blood sugars

A

Bendroflumethiazide works on the distal convoluted tubule to reduce both sodium and potassium reabsorption.
Insulin release from Beta cells is mediated in part by membrane ATP-sensitive potassium channels.

Due to low serum potassium there is therefore decreased insulin release and therefore worsening blood sugars

366
Q

what type of DI does lithium cause

A

nephrogenic DI

367
Q

what is Wolfram syndrome

A

aka DIDMOAD syndrome
DI (diabetes insipidus)
DM (diabetes mellitus)
OA (optic atrophy)
D (deafness)

368
Q

what is acarbose used for ad what is side effect

A

cam be used for T2DM but not as effective as other meds
Sid effects of GI upset / flatulence / bloating

369
Q

best Tx for postural hypotension

A

increase dietary NaCl

370
Q

next step in gestational diabetes if fasting palms glucose remains uncontrolled on diet, exercise and metformin

A

insulin

year 3 conditions (17 decks)

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