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Y6 Senior Med > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What is the function of insulin?

A

to drive glucose into cells when not needed

to inhibit ketone production when not needed

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2
Q

what are ketones need for?

A

to supply energy to brain during periods of hypoglycaema

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3
Q

what occurs during hypoglycaemia / starvation at hormone level

A

LOW insulin
HIGH glucagon / cortisol etc

this causes GLYCOGEN to be taken out of cells > converted back to GLUCOSE
KETONE production

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4
Q

What will fasting and OGTT tests be in T1DM

A

Fasting blood glucose >7

OGTT >11.1

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5
Q

what is normal, prediabetes and diabetes HbA1c

A

Normal: <42
Prediabetes: 42 - 48
Diabetes: >48

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6
Q

what are classical sx of diabetes and why?

A

TRIAD; fatigue, polyuria,polydipsia

as glucose is an osmotic diuretic, so it pulls out water

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7
Q

what are two classicAL presentations of diabetic neuropathy

A

Gastroparesis (vagus N neuropathy&raquo_space; erratic BMs, bloating, vomiting)&raquo_space; mx with metoclopramide

Neuropathic pain&raquo_space; mx with amyltryptiline

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8
Q

WHat is diabetic food secondary to?

A

neuropathy – loss of sensation

Peripheral arterial disease (due to reduced oxygen) – absent foot pulses, intermittent claudication

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9
Q

how do you check for diabetic foot neuropathy

A

10g monofilament test, done at least annually

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10
Q

how do you check for diabetic NEPHROPATHY

A

Yearly ACR (albumin : creatinine ratio)

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11
Q

what is the first sign of diabetic nephropathy=

A

microalbuminuria

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12
Q

what is the effect of ACEi on AKI, CKD and diabetic nephropathy

A

TOXIC in AKI

PROTECTIVE in CKD and diabetic nephropathy

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13
Q

when must you stop an ACEi

A

when there is a drop in GFR >20%

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14
Q

what is ACEi’s initial effect of GFR

A

initial drop due to dilating of the efferent arteriole

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15
Q

How often do you monitor cap glucose in T1 diabetes

A

4x a day in adults, 5x a day in children

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16
Q

How can you manage T1DM

A
  • BASAL BOLUS REGIMEN (rapid insulin with meal, long acting insulin BD)

OR

  • Twice daily BIPHASIC INSULIN (which is a mix of long and short acting)
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17
Q

When is basal bolus regimen most appropriatw

A

when patients are bale to count carbs and ensure that sufficient insulin is taken per meal

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18
Q

Give examples of short acting insulin

A

Actrapid

Novorapid

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19
Q

Give exaplines of long acting insulin

A

lantus

levemir

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20
Q

give example of mixed biphasic insulin

A

Humulim M3

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21
Q

What HbA1c do you start metforminn for? WHen do you escalate to dual therapy?

A

Start METFORMIN if HbA1c >48

DUAL THERAPY if HbA1c >58, aim for <53

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22
Q

How do you manage T2DM first line

A
  1. Metformin max 2g/day
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23
Q

What is MoA of metformin

A

increases insulin sensitivity

decreases hepatic gluconeogenesis

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24
Q

side effects of metformin

A

appetite suppression, diarrhoea, lactic acidosis

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25
Q

what do you do if metformin is causing diarrhoea

A

change to modified release

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26
Q

when is metformin contraindicated

A

if eGFR <30

if tissue hypoxia e.g. MI, surgery

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27
Q

When do you upscale to adding another drug to metformin

A

when HbA1c >58

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28
Q

what classes of drug can you add to metformin

A

sulphonylurea
thazolidinedione
gliptin
SGLT2 inhibitor

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29
Q

how do sulphonylureas work

A

by stimulating insulin production in the pancreease

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30
Q

side effects of sulphonylurea

A

weight gain, HYPOGLYCAEMIA

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31
Q

give examples of sulphonylurea

A

glibenclamide

gliclazide

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32
Q

what is method of action of gliptins

A

DPP4 inhibitor – stops the body from destroying incretin, which controls insulin production

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33
Q

give example of gliptin

A

SITAGLIPTIN

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34
Q

when is a sulphonylurea contraindicated

A

when patient is already fat

or if ketoacidotis

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35
Q

give example of SGLT 2 inhibitore

A

Empaglifloxin

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36
Q

What can you give if triple therapy for T2DM?

A

Metformin + sulphonyluria + other

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37
Q

what can you give for T2DM after triple therapy?

A

Metformin + sulphonylurea + GLP1 analogue

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38
Q

Why does HHS cause high glucose but not high ketones

A

because there is insufficient insulin to drive glucose into cells
but still enough insulin to inhibit ketone production

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39
Q

List causes of hyperthyroidism

A
  1. Graves disease
  2. Toxic multinodular goitre
  3. Toxic adenoma
    • these are high uptake on RI scan –
      4. Viral thyroiditis , subacute thyroiditis
      5. Post partum thyroiiditis
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40
Q

What occurs in Graves disease

A

Anti TSH R antibodies (igG)

This leads to increased thyroid function and thyroid growth

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41
Q

what are the three key SS of Graves disease

A
  1. Diffuse smoothlly enlarged GOITRE
  2. OPTHAMOPATHY (exomthalmos) (protruding eyes, due to THSr Ab on eye muscles)
  3. pretibial myxoedema

may also have LID LAG

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42
Q

How do you investigate suspected graves

A

T4, TSH serum
Anti TSH R Ab
Annti TPO Ab

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43
Q

How do you manage Graves

A
  1. Beta blocker PROPANOLOL ( to control sx)
  2. Anti thyroid drug (e.g. carbimazole, propilthiouracil) with aim of titrating down and stopping
  3. Radioiodine
  4. Surgery - last resort
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44
Q

causes of hypothyroidism

A
  1. Hashimotos
  2. Viral thyroiditis, post partum
  3. Iatrogenic
  4. Iodine deficiency
  5. Subclinical thyroiditis
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45
Q

What is Hashmoto’s

A

AI cause of HYPOTHYROIDsm

due to anti-TBO Ab

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46
Q

Iatrogenic causes of hypothyroidism

A

Post-graves disease (due to tx)

Drugs (amiodarone, lithium)

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47
Q

How do you manage hypothyroidism

A

Thyroxine - aim for normal TSH

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48
Q

what will extreme hypothyroidism cause and how does it present

A

it causes MYXOEDEMA COMA

presents as hypothermia, hyporeflexia, bradycardia, seizures

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49
Q

How do you manaage myxoedema coma

A

IV tyroxine
IV hydrocortisone
fluids

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50
Q

Where and what hormones are produced by the adrenal

A

ZG: Mineralocorticoids (ALDOSTERONE)
ZF: Glucocorticoids (Cortisol)
ZR: Androgeens
Medulla: Adrenaline, NA

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51
Q

What triggers production of cortisol

A

the HPA axis (CRH > ACTH >cortisol)

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52
Q

what is aldosterone produced in respnse to

A

increased sodium to KIDNEYS
decreaseed perfusion to kidneys
SNS axctivation

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53
Q

what can aldosterone bond to

A

Mineralocorticoid R

54
Q

What does aldosterone induce

A

SODIUM REABSORTPION > WATER REABSORPTION

POTASSIUM EXCRETION

55
Q

what is the fucntion of glucocorticoids

A

to regularte glucose balance

56
Q

What are causes of adrenal insufficiency

A

PRIMARY: Addison’s (AI) or TB, causing adrenal gland destruction

SECNODARY: Pituitary adenoma / sheehan’s

TERTIARY: brain tumour

57
Q

How does adrenal insufficiency prsent

A 
fatigue, anorxia, WL 
nausea, vomiting, abdo pain 
hyperpigmentation (raised ACTH) 
low BP (insufficient fluid and salt retention)
58
Q

How do you investigate adrenal insufficiency

A
  1. 9AM cortisol – if LOW: suspect

2. adminisrter short synachten test

59
Q

How do you manage adrenak insufficiency

A

Hydrocortisone (GC) and fludrocortisone (MC)

+ treat cause

60
Q

HJow do you manage acute addisonian crisis

A
  1. IM hydrocortisone&raquo_space; IV fluid bolus + glucose
61
Q

What are the two sizes of a pituitary adenoma

A

microadenoma <1cm

macroadenoma > 1cm

62
Q

Whayt is the commonest type of pituitary adenoma

A

PROLACTINNOMA

63
Q

presentation of prolactinoma

A

impotence, infertility, decreased libido, galactorrhoea, amenorrhoea, osteoporosis
depletion of hormones > hypopituitarism
headaches
bitemporal hemianopia

64
Q

prolactinoma mx

A

Bromocriptine, cabergolien

transnasal hypophysectomy

65
Q

what is cushings syndrome caused by

A

EXCESS CORTISOL

Exogenous GC therapy

Endogenous:

  • ACTH dependent (Cushings disease, ectopic ACTH production from SCLC)
  • ACTH independeenrt (steroids, adrenal adenoma, adrenal carcinoma)
66
Q

what is CUSHINGS DISEASE

A

Excess ACTH from pituitary gland, usually due to pituitary tumour

67
Q

Sx of cushings syndrome

A 
personality changes, irritability 
rounded face 
interscapular fat pad 
gynaecomastia (men ) 
purple striae, thin skin, easy bruising , petechiae 
increaseed susceptibility to infectionn 
osteoporosis
PROXIMAL MYOPATHY
68
Q

Ix for Cushings syndrome

A
  1. 11pm salivary cortisol (if low, not cushing’s)
  2. LDDST
  3. Inferior petrosal sinus sampling (identifies pituitary disease)
69
Q

What does LDDST show

A

after dexamethason:

  • if cortisol is low > normal suppression
  • if cortisol is still high > confirmed Cushings synsrome, perfomr IPSS
70
Q

How do you manage pituitary adenoma

A

surgical removal

71
Q

How do you manage adrenal mass causing Cushing syndrome

A

Adrenalectomy + steroid replacement

72
Q

What is Conns syndrome

A

Excess ALDOSTERONE ONLY > excess salt and water reabbsorption, excess potassium excretion

73
Q

causes of Conns syndrome

A 
adrenal adenoma 
adrenal hyperplasia (bilateral)
74
Q

How does Conns present

A

HTN refractory to tx

hypokalaemia (muslce weakness, parasthesia, tetany)

75
Q

How do you ix Conns

A

Plasma aldosterone / renin ratio

76
Q

What is Plasma aldosterone / renin ratio like in Conns

A
  • result in Conns will be HIGH as very high aldosterone switches off renin production
77
Q

What is Plasma aldosterone / renin ratio like in RAS

A

ARR normal

becuase it is the high renin that raises aldosterone

78
Q

How do you manaage CONNS

A

spironolactonee / eplerenone > surgery

avoid surgery in elderly

79
Q

How does PTH control calcum

A

HIGH PTC causes:

  • increased Ca resorption in bone
  • increased Ca absorption in GI
  • decreaseed Ca excretion in kidney
  • increased 1alpha hydroxylase&raquo_space; activates vit D
80
Q

how does PTH affect vit D

A

It causes activation of Vit D to 1,25OH2D

by triggering 1a hydroxylase production in kindey

81
Q

what does 1,25(OH)2D cause

A

increased Ca absorption in GI

Decreased excretion of Ca in kidney

82
Q

what must you check first in hypercalcaemia

A

PTH serum

83
Q

what does PTH in ypercalacemia tell you

A

Low PTH: hypercalcaemia of malignancy

  • bone mets
  • PTH producing Squamous cell carcinoma of lunng
  • myeloma

Normal/high PTH: PRIMARY HYPERPARATHYROIDISM

  • PT carcinoma
  • adenoma
  • hyperplasia
84
Q

Symptoms of hypercalcaemia

A

Bone pain, fractures
Stones - renal stones
abdo groans - peptic ulcer, constipation, pancreatitis, polyuria, poluyfipssia
psychic moans - depression

85
Q

How do you treat hypercalcaemA

A

fluids 3-4 L/day
biphosphonates if bone mets
treat cause

86
Q

what is secondary hyperparathyroidism and why does it occur

A

raised PTH due to LOW calcium

caused by:

  • chronic renal failure
  • vit D deficiency
87
Q

what is tertiary hyperparathyroidism

A

continously raised PTH even once calcium normalises / becomes high +
due to end stage renal failure

88
Q

how do you manage tertiary HPT

A

parathyroidectomy

89
Q

what are blood results in pagets

A

raised ALP
everything lse normal

because this is a disease of excessive bone turnover

90
Q

causees of B12 deficiency

A

Pernicious anaemia (AI)
Atrophic gastritis
Gastrectomy
Malnutrition

91
Q

Signs of B12 deficiiency

A

Anaemia (lethargy, pallor, dyspnoea)
Neuro (peripheral neuropathy, weakness, ataxia, parasthesia)
Glossitis
Mild jaundicee

92
Q

Ix for B12 deficiency

A

FBC (macrocytic anaemia, hypersecomented neutrophils)
b12 level
Anti IF Ab
Anti parital cell antibodies

93
Q

management B12 deficiency

A

Severe: IM vitamin B12 (hydroxycobalamin, 3x weekly for 2 weeks, then three monthly injections)
Mild-moderate: PO / IM B12

94
Q

How does subclinical hypothyroidims present on biochemistry?

A

High TSH

Normal T4

95
Q

what do you do with someone presenting with subclinical hypothyroidism

A

Repeat bloods in 6 weeks

96
Q

What do you do if repeat TSH is elevated in subclin hypothyroidism?

A

TSH >10 : levothyroxin
TSH 5-10 + postive autoantibodies : repeat bloods in 1 year
TSH 5-10 and -ve antibodies : repeat bloods in 3-5 years

97
Q

causes of HYPOCALCAEEMIA

A
  1. PTH failure
  2. Low vit D
  3. Pancreatitis
  4. Hypomagnesaemia
98
Q

How do you investigate a thyroid neck lump that you are concerned about?

A
  • TFT
  • thyroid autoaantibodies
  • Thryoid USS +- fine needle aspirate
  • thyroid uptake scan
99
Q

how do ytou manage thyroid cancer

A

hemi thyroidectomy + iodinine

100
Q

side effect of carbimazole

A

neutropoenia

101
Q

what is contraindication of giving radioiodine in graves disease

A

contraindicated in pregnancy or eye disease

102
Q

what is complication of surgery to treat Graves

A

damage to recurrent laryngeal nerve > hoarseness

103
Q

causes of HYPERNATRAEMIA

A

DEHYDRATON - LOSS OF WATER

  • GI loss
  • Sweat loss
  • Renal loss (diabetes insipidus, diabetes mellitus)

INCREASE IN SODIUM

  • iatrogenic
  • high dietary intake
  • Conn’s
  • RAS
104
Q

How do you tell apart Conn’s drom RAS

A

Using aldosterone : renal ratio

in CONNS, ARR is HIGH
In RAS, it is normal

105
Q

how do you invesrigate HYPERnatraemiia

A

volume state - physical examination

  • serum glucose (exclude diabetes)
  • serum K+ (raised > Conn’s. Low > nephrogenic DI)
  • plasma and urine osmolarity (hyperaldosteronism: high plasma osmolarity)
  • Water deprivation test (diabetes insipidus()
106
Q

what test can you do for diabetes insipiitdu

A

water deprivation test

  • neurogenic responds to ddavp
  • nephrogenic does NOT respond
107
Q

How do you treat hypernatraemia

A

Correct water deficit if dehydrated with 1L 5% dextrose IV over 8-10h
treat cause

108
Q

complications of hypernatraemia

A

RAPID HYPERnatraemia correction> cerebral oedema

109
Q

causes of HYPONATRAEMIA (by fluid status)

A

HYPOVOLAEMIC:

  • diarrhoea
  • vomiting
  • diuretics

EUVOLAEMIC: (E=endocrine)

  • SIADH
  • Hypothyroid
  • Adrenal insufficiency

HYPERVOLAEMIA: (overloaded = organ failure)

  • liver failure
  • CCF
  • renal failure
110
Q

what occurs physiologically in the kidneys if hypovolaemic and how does it affect sodium concentration?

A

kidneys increase sodium reeabsorption
this draws in water
this decreases urinary sodium

111
Q

How can we interpret urinary sodium in the context of hyponatraemia

A

urinary sodium LOW: this is due to hypovolaemic state (kidneys functioning as normal)

urinary sodium HIGH (above 20): SIADH

112
Q

what are the two hormones that regulate sodium absorption

A

aldosterone

ADH

113
Q

how does aldosterone work

A

bids to Mineralocorticoid R

Increases NA reabsorption> pulls in water

114
Q

how does ADH work

A

inserts aquaporin channels > water reabsorption

115
Q

what mx required in hyponatraemia?=

A

HYPOVOLAEMIC: IV fluids (0.9% saline) slowly
Euvolaemic / HYPERvolaemic: fluid restrict + treat cause

SEVERE hyponatraemia <120 : 3% isotonic saline

116
Q

what do you do if patient is severely hyponatramemiic (<120)

A

slow 3% salin

117
Q

what drugs can you give for SIADH

A

Demeclocycline (induce nephrogenic DI, reducing responsiveness of collecting tubes to ADH )
Tolvaptan (V2 receptor antagonist)

118
Q

what ix do you do for SIADH

A

plasma osmolarity and urine osmolarity

plasma will be low, urine will be high

119
Q

complication of treating hyPOnatraemia too fast

A

cerebral POntine myelinolysis

120
Q

Causes of HYPERkalaemia

A

DECREASED RENAL POTASSIUM EXCRETION

  • Low GFR (poor kidney functon> insufficient K excreton)
  • Low renin (T24 RTA, NSAIDS)
  • ACEi
  • ARBs
  • Addison’s (no aldosterone > no K+ excretion)
  • Aldosterone antagonist (counters aldosterone effect, eg spironolactone)

INCREASED POTASSIUM RELEASE FROM CELLS

  • rhabdo
  • acidosis
121
Q

summartise drugs that cause HYPERKALAEMIA

A

NSAIDS
ACE i
ARBs
Spironolactone

122
Q

Whhat is presentation of hyperkalaemic pt

A

muscle weakness and lethargy
fatigue
parasthesia
palpitations

123
Q

ECG in hyperkalaemia

A 
TALL N TENTED T WAVE 
Broad QRS 
Flat P wave 
Prolonged PR interval 
Eventual SINE WAVE > > cardiac arrest
124
Q

causes of HYPOKALAEMIA

A
  • GI loss (diarrhoea)
  • renal loss (loop and thiazide diuretics, excess MR with Conns, Cushings)
  • redistribution into cells (insulin / insulinomas, beta agonists, alkalosis)
125
Q

mx hypokalaemia

A

K+ >2.5: 2 sandoK tablets TDS for 48h

K+ <2.5 or symptoms /ECG: 3x 1L NaCl with 40mmol KCL over 24h

126
Q

sick euthyroid cause

A

acute illness – abnormal thyroidd results but will normalise oncee illness resolves

127
Q

sick euthyroid biochemistry

A

Normal or low TSH

low T3 and T4

128
Q

how do you investigate acromegaly

A

serum IGF1

to confirm dx, do an OGTT with GH measurement

129
Q

what do you need to give in refeeding syndrome

A

phosphate

130
Q

causes of SIADH

A

CNS pathology - stroke, haemorrhage, tumour
Lung pathology - pneumonia, pneumothorax
Drugs - SSRI, TCA, carbamazepine, sulphonylurea
Tumour
Surgery

131
Q

what occurs with SIADH

A

Excess ADH > increased water retention > increased volume >RAAS suppressed > less aldosterone > less water absorption

So HYPOnatraemia with EUvolaemia

132
Q

how do you treat MODY

A

MODY is very sensitive to sulphonylureas

Y6 Senior Med (29 decks)

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