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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
what do you do if metformin is causing diarrhoea
change to modified release
26
when is metformin contraindicated
if eGFR <30 | if tissue hypoxia e.g. MI, surgery
27
When do you upscale to adding another drug to metformin
when HbA1c >58
28
what classes of drug can you add to metformin
sulphonylurea thazolidinedione gliptin SGLT2 inhibitor
29
how do sulphonylureas work
by stimulating insulin production in the pancreease
30
side effects of sulphonylurea
weight gain, HYPOGLYCAEMIA
31
give examples of sulphonylurea
glibenclamide | gliclazide
32
what is method of action of gliptins
DPP4 inhibitor -- stops the body from destroying incretin, which controls insulin production
33
give example of gliptin
SITAGLIPTIN
34
when is a sulphonylurea contraindicated
when patient is already fat | or if ketoacidotis
35
give example of SGLT 2 inhibitore
Empaglifloxin
36
What can you give if triple therapy for T2DM?
Metformin + sulphonyluria + other
37
what can you give for T2DM after triple therapy?
Metformin + sulphonylurea + GLP1 analogue
38
Why does HHS cause high glucose but not high ketones
because there is insufficient insulin to drive glucose into cells but still enough insulin to inhibit ketone production
39
List causes of hyperthyroidism
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
40
What occurs in Graves disease
Anti TSH R antibodies (igG) | This leads to increased thyroid function and thyroid growth
41
what are the three key SS of Graves disease
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
42
How do you investigate suspected graves
T4, TSH serum Anti TSH R Ab Annti TPO Ab
43
How do you manage Graves
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
44
causes of hypothyroidism
1. Hashimotos 2. Viral thyroiditis, post partum 3. Iatrogenic 4. Iodine deficiency 5. Subclinical thyroiditis
45
What is Hashmoto's
AI cause of HYPOTHYROIDsm | due to anti-TBO Ab
46
Iatrogenic causes of hypothyroidism
Post-graves disease (due to tx) | Drugs (amiodarone, lithium)
47
How do you manage hypothyroidism
Thyroxine - aim for normal TSH
48
what will extreme hypothyroidism cause and how does it present
it causes MYXOEDEMA COMA presents as hypothermia, hyporeflexia, bradycardia, seizures
49
How do you manaage myxoedema coma
IV tyroxine IV hydrocortisone fluids
50
Where and what hormones are produced by the adrenal
ZG: Mineralocorticoids (ALDOSTERONE) ZF: Glucocorticoids (Cortisol) ZR: Androgeens Medulla: Adrenaline, NA
51
What triggers production of cortisol
the HPA axis (CRH > ACTH >cortisol)
52
what is aldosterone produced in respnse to
increased sodium to KIDNEYS decreaseed perfusion to kidneys SNS axctivation
53
what can aldosterone bond to
Mineralocorticoid R
54
What does aldosterone induce
SODIUM REABSORTPION > WATER REABSORPTION | POTASSIUM EXCRETION
55
what is the fucntion of glucocorticoids
to regularte glucose balance
56
What are causes of adrenal insufficiency
PRIMARY: Addison's (AI) or TB, causing adrenal gland destruction SECNODARY: Pituitary adenoma / sheehan's TERTIARY: brain tumour
57
How does adrenal insufficiency prsent
``` fatigue, anorxia, WL nausea, vomiting, abdo pain hyperpigmentation (raised ACTH) low BP (insufficient fluid and salt retention) ```
58
How do you investigate adrenal insufficiency
1. 9AM cortisol -- if LOW: suspect | 2. adminisrter short synachten test
59
How do you manage adrenak insufficiency
Hydrocortisone (GC) and fludrocortisone (MC) | + treat cause
60
HJow do you manage acute addisonian crisis
1. IM hydrocortisone >> IV fluid bolus + glucose
61
What are the two sizes of a pituitary adenoma
microadenoma <1cm | macroadenoma > 1cm
62
Whayt is the commonest type of pituitary adenoma
PROLACTINNOMA
63
presentation of prolactinoma
impotence, infertility, decreased libido, galactorrhoea, amenorrhoea, osteoporosis depletion of hormones > hypopituitarism headaches bitemporal hemianopia
64
prolactinoma mx
Bromocriptine, cabergolien | transnasal hypophysectomy
65
what is cushings syndrome caused by
EXCESS CORTISOL Exogenous GC therapy Endogenous: - ACTH dependent (Cushings disease, ectopic ACTH production from SCLC) - ACTH independeenrt (steroids, adrenal adenoma, adrenal carcinoma)
66
what is CUSHINGS DISEASE
Excess ACTH from pituitary gland, usually due to pituitary tumour
67
Sx of cushings syndrome
``` 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
Ix for Cushings syndrome
1. 11pm salivary cortisol (if low, not cushing's) 2. LDDST 3. Inferior petrosal sinus sampling (identifies pituitary disease)
69
What does LDDST show
after dexamethason: - if cortisol is low > normal suppression - if cortisol is still high > confirmed Cushings synsrome, perfomr IPSS
70
How do you manage pituitary adenoma
surgical removal
71
How do you manage adrenal mass causing Cushing syndrome
Adrenalectomy + steroid replacement
72
What is Conns syndrome
Excess ALDOSTERONE ONLY > excess salt and water reabbsorption, excess potassium excretion
73
causes of Conns syndrome
``` adrenal adenoma adrenal hyperplasia (bilateral) ```
74
How does Conns present
HTN refractory to tx | hypokalaemia (muslce weakness, parasthesia, tetany)
75
How do you ix Conns
Plasma aldosterone / renin ratio
76
What is Plasma aldosterone / renin ratio like in Conns
- result in Conns will be HIGH as very high aldosterone switches off renin production
77
What is Plasma aldosterone / renin ratio like in RAS
ARR normal | becuase it is the high renin that raises aldosterone
78
How do you manaage CONNS
spironolactonee / eplerenone > surgery | avoid surgery in elderly
79
How does PTH control calcum
HIGH PTC causes: - increased Ca resorption in bone - increased Ca absorption in GI - decreaseed Ca excretion in kidney - increased 1alpha hydroxylase >> activates vit D
80
how does PTH affect vit D
It causes activation of Vit D to 1,25OH2D | by triggering 1a hydroxylase production in kindey
81
what does 1,25(OH)2D cause
increased Ca absorption in GI | Decreased excretion of Ca in kidney
82
what must you check first in hypercalcaemia
PTH serum
83
what does PTH in ypercalacemia tell you
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
Symptoms of hypercalcaemia
Bone pain, fractures Stones - renal stones abdo groans - peptic ulcer, constipation, pancreatitis, polyuria, poluyfipssia psychic moans - depression
85
How do you treat hypercalcaemA
fluids 3-4 L/day biphosphonates if bone mets treat cause
86
what is secondary hyperparathyroidism and why does it occur
raised PTH due to LOW calcium caused by: - chronic renal failure - vit D deficiency
87
what is tertiary hyperparathyroidism
continously raised PTH even once calcium normalises / becomes high + due to end stage renal failure
88
how do you manage tertiary HPT
parathyroidectomy
89
what are blood results in pagets
raised ALP everything lse normal because this is a disease of excessive bone turnover
90
causees of B12 deficiency
Pernicious anaemia (AI) Atrophic gastritis Gastrectomy Malnutrition
91
Signs of B12 deficiiency
Anaemia (lethargy, pallor, dyspnoea) Neuro (peripheral neuropathy, weakness, ataxia, parasthesia) Glossitis Mild jaundicee
92
Ix for B12 deficiency
FBC (macrocytic anaemia, hypersecomented neutrophils) b12 level Anti IF Ab Anti parital cell antibodies
93
management B12 deficiency
Severe: IM vitamin B12 (hydroxycobalamin, 3x weekly for 2 weeks, then three monthly injections) Mild-moderate: PO / IM B12
94
How does subclinical hypothyroidims present on biochemistry?
High TSH | Normal T4
95
what do you do with someone presenting with subclinical hypothyroidism
Repeat bloods in 6 weeks
96
What do you do if repeat TSH is elevated in subclin hypothyroidism?
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
causes of HYPOCALCAEEMIA
1. PTH failure 2. Low vit D 3. Pancreatitis 4. Hypomagnesaemia
98
How do you investigate a thyroid neck lump that you are concerned about?
- TFT - thyroid autoaantibodies - Thryoid USS +- fine needle aspirate - thyroid uptake scan
99
how do ytou manage thyroid cancer
hemi thyroidectomy + iodinine
100
side effect of carbimazole
neutropoenia
101
what is contraindication of giving radioiodine in graves disease
contraindicated in pregnancy or eye disease
102
what is complication of surgery to treat Graves
damage to recurrent laryngeal nerve > hoarseness
103
causes of HYPERNATRAEMIA
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
How do you tell apart Conn's drom RAS
Using aldosterone : renal ratio in CONNS, ARR is HIGH In RAS, it is normal
105
how do you invesrigate HYPERnatraemiia
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
what test can you do for diabetes insipiitdu
water deprivation test - neurogenic responds to ddavp - nephrogenic does NOT respond
107
How do you treat hypernatraemia
Correct water deficit if dehydrated with 1L 5% dextrose IV over 8-10h treat cause
108
complications of hypernatraemia
RAPID HYPERnatraemia correction> cerebral oedema
109
causes of HYPONATRAEMIA (by fluid status)
HYPOVOLAEMIC: - diarrhoea - vomiting - diuretics EUVOLAEMIC: (E=endocrine) - SIADH - Hypothyroid - Adrenal insufficiency HYPERVOLAEMIA: (overloaded = organ failure) - liver failure - CCF - renal failure
110
what occurs physiologically in the kidneys if hypovolaemic and how does it affect sodium concentration?
kidneys increase sodium reeabsorption this draws in water this decreases urinary sodium
111
How can we interpret urinary sodium in the context of hyponatraemia
urinary sodium LOW: this is due to hypovolaemic state (kidneys functioning as normal) urinary sodium HIGH (above 20): SIADH
112
what are the two hormones that regulate sodium absorption
aldosterone | ADH
113
how does aldosterone work
bids to Mineralocorticoid R | Increases NA reabsorption> pulls in water
114
how does ADH work
inserts aquaporin channels > water reabsorption
115
what mx required in hyponatraemia?=
HYPOVOLAEMIC: IV fluids (0.9% saline) slowly Euvolaemic / HYPERvolaemic: fluid restrict + treat cause SEVERE hyponatraemia <120 : 3% isotonic saline
116
what do you do if patient is severely hyponatramemiic (<120)
slow 3% salin
117
what drugs can you give for SIADH
Demeclocycline (induce nephrogenic DI, reducing responsiveness of collecting tubes to ADH ) Tolvaptan (V2 receptor antagonist)
118
what ix do you do for SIADH
plasma osmolarity and urine osmolarity | plasma will be low, urine will be high
119
complication of treating hyPOnatraemia too fast
cerebral POntine myelinolysis
120
Causes of HYPERkalaemia
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
summartise drugs that cause HYPERKALAEMIA
NSAIDS ACE i ARBs Spironolactone
122
Whhat is presentation of hyperkalaemic pt
muscle weakness and lethargy fatigue parasthesia palpitations
123
ECG in hyperkalaemia
``` TALL N TENTED T WAVE Broad QRS Flat P wave Prolonged PR interval Eventual SINE WAVE > > cardiac arrest ```
124
causes of HYPOKALAEMIA
- GI loss (diarrhoea) - renal loss (loop and thiazide diuretics, excess MR with Conns, Cushings) - redistribution into cells (insulin / insulinomas, beta agonists, alkalosis)
125
mx hypokalaemia
K+ >2.5: 2 sandoK tablets TDS for 48h | K+ <2.5 or symptoms /ECG: 3x 1L NaCl with 40mmol KCL over 24h
126
sick euthyroid cause
acute illness -- abnormal thyroidd results but will normalise oncee illness resolves
127
sick euthyroid biochemistry
Normal or low TSH | low T3 and T4
128
how do you investigate acromegaly
serum IGF1 to confirm dx, do an OGTT with GH measurement
129
what do you need to give in refeeding syndrome
phosphate
130
causes of SIADH
CNS pathology - stroke, haemorrhage, tumour Lung pathology - pneumonia, pneumothorax Drugs - SSRI, TCA, carbamazepine, sulphonylurea Tumour Surgery
131
what occurs with SIADH
Excess ADH > increased water retention > increased volume >RAAS suppressed > less aldosterone > less water absorption So HYPOnatraemia with EUvolaemia
132
how do you treat MODY
MODY is very sensitive to sulphonylureas

Y6 Senior Med (29 decks)

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