Endocrinology Flashcards

1
Q

Complications of Acromegaly (4)

A

Hypertension
Diabetes (>10%)
Cardiomyopathy
Colorectal cancer

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2
Q

First line test for Acromegaly and monitoring of disease:

A

Serum IGF-1 levels (no longer OGTT)

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3
Q

Test to confirm Acromegaly if IGF-1 raised:

A

OGTT

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4
Q

First line treatment Acromegaly:

A

Trans-sphenoidal surgery

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5
Q

Medical management of Acromegaly if surgery unsuitable:

A

Somatostatin analogue - inhibits release of GH (Octreotide)

Pegvisomant (GH receptor antagonist)

Dopamine antagonists (bromcriptine)

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6
Q

Addisons disease electrolyte imbalance:

A

HYPOnatraemia
HYPERkalaemia
HYPOglycaemia

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7
Q

Difference between primary Addisons and secondary Addisons (appearance)

A

Primary (adrenal cause) will cause HYPERPIGMENTATION, secondary (pituitary causes) will not.

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8
Q

Addisons investigation of choice:

A

ACTH (short synacthen test)

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9
Q

What is measured with ACTH stimulation test (synacthen test)

A

CORTISOL before and 30 minutes after administration of ACTH

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10
Q

Levels of 9 am cortisol in Addisons if ACTH test not available:

A

<100 = definitely abnormal
>500 Unlikely Addison’s
100-500 get SYNACTHEN test

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11
Q

Addison’s adrenal autoantibody:

A

Anti-21 hydroxylase

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12
Q

Addisons treatment:

A

Hydrocortisone and fludrocortisone

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13
Q

If concurrent illness in pre-established Addisons: what are you going to regarding steroids:

A

DOUBLE hydrocortisone

Keep fludrocortisone the same

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14
Q

Addisonian crisis management:

A

Hydrocortisone
1L saline with dextrose if hypoglycaemic
NO FLUDROCORTISONE IS REQUIRED as high cortisol exerts weak mineralocorticoid activity

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15
Q

Bartter’s syndrome condition which acts like taking which drug:

A

Large doses of LOOP diuretic (hypokalaemia, normotesnion)

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16
Q

Hypomaganesaemia may cause which other electrolyte disturbance:

A

Hypocalcaemia

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17
Q

Causes of congenital adrenal hyperplasia:

A

21–hydroxylase deficiency (90%)

11-B hydroxylase deficiency (5%)

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18
Q

Adrenal hyperplasia:
Androgens
Cortisol level:
ACTH level:

A

Low cortisol
High ACTH
High Androgens - Virilization of females, precocious puberty in males

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19
Q

Steroid FBC disturbance:

A

Neutrophilia (may seem paradoxical due to immuno-suppressive nature of drug)

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20
Q

When should steroids be withdrawn gradually:

A

If pt. has

  • received more than 40mg/day for more than 1 week
  • received more than 3 weeks of treatment
  • recently received repeated courses
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21
Q

Cushing’s syndrome electrolyte disturbance:

A

hypokalaemic metabolic alkalosis with impaired glucose tolerance.

Think of (for memory) : increased cortisol, increased aldosterone = increased Na retention and subsequent K loss -> K is positively charged, Pro-acidotic thus loss will = alkalosis.

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22
Q

First-line test for confirming Cushing’s syndrome:

A

Overnight dexamethasone suppression test

Cushing’s pts. will not have their cortisol morning spike suppressed.

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23
Q

Localisation test for Cushing’s:

A

High dose Dexamethasone suppression test

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24
Q

Localisation tests for Cushing’s:
Cortisol: NOT supressed
ACTH: suppressed
Interpretation:

A

Cushing’s syndrome (adrenal problem)

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25
Localisation tests for cushings: Cortisol: Suppressed ACTH: Suppressed Interpretation:
Cushing's disease (ACTH pituitary adenoma)
26
Localisation tests for cushings: Cortisol: NOT supressed ACTH: NOT suppressed Interpretation:
Ectopic ACTH syndrome
27
Test to differentiate between Cushings and pseudo-Cushing's
Insulin stress test
28
Test to differentiate between Pituitary and Ectopic ACTH production
Petrosal sinus sampling
29
T1DM antibodies
anti-GAd (80%) | Islet cell antibodies (ICA) (70%)
30
T1DM diagnostic blood glucose levels
``` Fasting (>7) Random glucose (11.1) or after 75g glucose tolerance test ```
31
If diagnostic doubt between T1DM and T2DM which test would you use?
C-peptide levels (low in T1) and specific autoantibodies
32
HBA1c should be checked:
Every 3-6 months till stable then 6 monthly
33
HBA1c targets:
Lifestyle - 48 Lifestyle + metformin - 48 includes drug which can cause hypoglycaemia (e.g sulphonylurea) - 53 Patient already on treatment: but has risen to 58 mmol - 53
34
Only add second drug at what HBA1c
58
35
GLP-1 mimetic example
Exenatide
36
GLP-1 mimetic (exenatide) criteria | only continued if:
if triple therapy not effective: consider Metformin, SU and GLP-1 if: BMI > 35 BMI <35 but insulin would have adverse effect on ADLs or QoL Only continued if wt.loss of 3% total in 6 months or reduction in HBA1c of 11
37
T2DM > 80 years old blood pressure target
150/90
38
Pre-diabtes HBA1c: Fasting glucose:
42-47 | 6.1-6.9
39
Meformin side effects: | Cannot be offered with GFR of less than:
Lactic acidosis GI upset | >30
40
Sulphonylurea electrolyte disturbance:
Hyponatraemia
41
Thiazolidinediones side effects:
Weight gain | Fluid retention
42
GLP-1 (Exenatide) side effects:
Nausea and vomiting | Pancreatitis
43
Which diabetic drugs may cause weight loss:
GLP-1 agoinst and SGLT2 inhibitors
44
Which insulin should be offered in T1DM -
Multiple daily basal bolus insulin regimen | twice daily insulin determir is the regime of choice.
45
How many times a day should you test blood glucose; T1DM
4
46
When should you conisder adding metformin in T1DM
if BMI > 25
47
Exception for stopping oral anti-diabetic medications on sick-day
If very dehydrated, metformin should be stopped due to effect on renal function.
48
What is DKA caused by:
LIPOLYIS = increased free fatty acids which are converted to ketones
49
Management of DKA:
Fluid replacement (isotonic saline) Insulin (IV 0.1 unit/kg/hour) once blood glucose <15, dextrose (5%) may be commenced Correction of electrolyte disturbances (potassium may need replaced due to insulin-inudced hypokalemia)
50
DKA pt. regular insulin: what should be done?
Long-acting insulin continued, short-acting stopped
51
DKA resolution:
pH >7.3 blood ketones < 0.6 Bicarbonate > 15
52
Diabetic neuropathy first line treatment:
Amitryptiline, duloxetine, gabapentin or pregablin
53
Drug used as rescue therapy in neuropathic pain:
Tramadol
54
Causes of lower than expected HBA1c (due to reduced RBC lifespan)
Sickle cell anaemia G6PD deficiency Hereditary spherocytosis
55
Causes of higher than expected HBA1c (due to increased RBC lifespan)
VitB12/folate deficiency Iron-deficiency anaemia Splenectomy
56
Graves disease thyroid scintigraphy:
Diffuse homogenous increased uptake of radioactive iodine
57
Graves disease initial treatment to control symptoms
Propranolol
58
ATD (antithyroid drug) therapy:
2 options CARBIMAZOLE 40 mg then reduced till euthyroid Block and replace (40mg carbimazole then thyroxine at euthyroid can be used for 6-9 months)
59
IF ATD therapy is not working:
Radioiodine treatment - many require thyroxine supplementation after 5 years
60
Hashimotos associations:
Other autoimmune conditions (coeliac, T1DM, vitiligo) | MALT lymphoma
61
HHS result of increased serum osmolality (osmotic diuresis)
blood hyperviscosity - clot risk
62
Key parameter to monitor in HHS fluid replacement therapy
Serum osmolality
63
Goals of management in HHS:
1) Normalise the osmolality (gradually) 2) Replace fluid and electrolyte losses 3) Normalise blood glucose (gradually)
64
Management of hypoglycaemia in Community: Hospital (alert vs. non-alert):
Initially oral glucose 10-20g in liquid gel or tablet. If alert - short acting carbohydrate should be given If unconscious or unable to swallow - SC or IM GLUCAGON may be given Alternatively IV 20% glucose solution may be given through large vein
65
Primary hypoparathyroidism treatment
Alfacalcidol
66
Pseudohypoparathyroidism - due to target cells being insensitive to PTH - calcium, phosphate and PTH levels Clinical features:
low calcium, high phosphate, HIGH PTH Low IQ, short and shortened 4th and 5th metacarpals
67
pseudopsuedohypoparathyroidism
same as psuedoPTH with normal biochemistry
68
Hypothyroidism - when should lower starting dose of levothyroxine be used:
Elderly or pts. with ischaemic heart disease standard dose is 50-100 mcg od)
69
Therapeutic goal of thyroid therapy:
Normalisation of TSH (not thyroxine)
70
Pregnant women should have their dose of thyroxine..
Increased by 25-50 mcg
71
Side effects of thyroxine therapy:
Hyperthyroidism Reduced bone mineral density Worsening of angina (think about ischaemic heart disease in dosing) Atrial fibrillation.
72
Thyroxine interacts with
Iron and Calcium carbonate - give at least 4 hours apart
73
pro-insulin is cleaved to form:
Insulin and C-peptide
74
Insulin stress test: what should happen to cortisol and GH
They should both rise
75
Which cardio drug reduces hypoglycaemic awareness
Beta-blockers
76
Insulinoma: insulin/proinsulin findings
High insulin | Raised proinsulin:insulin ratio
77
Insulinoma Dx. Mx.
Supervised long fast (72 hours) CT pancreas Diazoxide and somatostatin used if patient not for surgery
78
Kallman's syndrome Give away: Levels of sex hormone:
Lack of smell Sex hormone levels usually low LH/FSH typically low/normal
79
Klinefelter's syndrome Karyotype: Features: Diagnosis by
47 XXY Often taller than average Small firm testes Gynaecomastia Elevated gonadotrophin but LOW testosterone Chromosome analysis
80
Liddle's syndrome | electrolyte imbalance:
Hypokalaemic alkalosis (increased absorption of sodium) Hypertension
81
Meglitinides MoA Good for pts. with what kind of lifestyle? Adverse effects:
Examples: Repaglinide, nateglinide work like SUs to INCREASE pancreatic insulin secretion Erratic lifestyles Weight gain and hypoglycaemia (but less than SUs)
82
What is MODY Inheritance Treatment:
T2DM in a person of <25 years. Autosomal dominant Pts. V sensitive to SUs Insulin not usually necessary
83
MEN I conditions Most common px. Oncogene: MEN1
3 Ps Parathyroid (hyperparathyroidism) Pituitary adenoma Pancreas (insulinoma, gastronoma -> recurrent peptic ulceration HYPERCALCAEMIA
84
MEN II: Oncogene:
2Ps, 1M Medullary Thyroid carcinoma Parathyroid Phaeochromocytoma RET oncogene
85
MEN IIb
Medullary thyroid cancer Phaechromocytoma Marfans Neuromas RET oncogene
86
Myxoedema coma px:
Confusion and HYPOTHERMIA
87
Myxoedema coma treatment:
``` IV thyroid replacement IV fluid IV corticosteroids correct electrolytes occasionally, rewarming ```
88
Neuroblastoma most commonly arises from =: Ix.
Adrenal medulla Raised urinary vanillylmandelic acid (VMA) and homovanillic acid (HVA) Calcification on x-ray Biopsy
89
Orlistat prescription requirements:
BMI > 28 w/ assoc. risk factors BMI > 30 Continued wt. loss - 5% at 3 months Orlistat usually used for <3 months
90
1ry hyperparathyroidism indications for surgery :
``` Elevated calcium (>1mg/dl) Hypercalciuria (>400mg/day) Creatinine clearance < 30% of normal Nephrolithiasis Age < 50 years Reduction in bone density ```
91
Tertiary hyperparathyroidism:
Occurs as a result of ongoing hyperplasia of the PTH glands after correction of underlying renal disorder.
92
Secondary hyperparathyroidism:
Renal failure
93
Distinguishing primary hyperparathyroidism and FHH:
Urine calcium: creatinine clearance ratio <0.01 points towards FHH
94
Phaeochromocytoma test:
24 hour urinary collection of METANEPHRINES (not catecholamines)
95
Phaechromocytoma Defnintive management: Stabilisation management
Surgery Alpha blocker GIVEN BEFORE Beta blocker
96
Pituitary blood profile:
GH, Prolactin, ACTH, FH, LSH, TFTs
97
First-line medical management for Prolactinomas surgery:
Dopamine agonist - Bromocriptine If progression in size, transphenoidal surgery may be used
98
Two types of impaired glucose regulation:
Impaired fasting glucose (IFG): Due to hepatic insulin resistance. Impaired glucose tolerance (IGT): due to muscle insulin resistance. IGT are more likely to develop T2DM and CV disease
99
Is there an increase in thyroxine in pregnancy:
Technically yes as increase in TBG = increase in total thyroxine But this does not affect the free thyroxine level.
100
ATDs in pregnancy
1st trimester PTU | 2nd/3rd trimester Carbimazole
101
Can you breastfeed on thyroxine:
Yes
102
Primary hyperaldosteronism | Electrolyte disturbance:
Hypertension, Hypokalaemia - muscle weakness Alkalosis
103
Primary hyperaldosteronism | Ix:
1) Plasma Aldosterone/renin ratio is first line (high aldosterone, low renin) 2) High resolution CT and adrenal vein sampling is used to differentiate between unilateral and bilateral causes If CT is normal, AVS used to distinguish between unilateral adenoma and bilateral hyperplasia
104
Primary hyperaldosteronism. | tx.
Adrenal adenoma: surgery Bilateral adrenocortical hyperplasia: Spironolactone
105
Hyperparathyroidism sign on X-ray:
Pepperpot skull
106
Hyperparathyroidism treatment:
Parathyroidectomy conservative management may be offered if calcium < 0.25 above normal and pt. > 50 years and no evidence of end organ damage Calcimimetic (circlet) may be used for those unsuitable for surgery
107
Prolactin is under constant inhibition by:
Dopamine
108
Drugs which can increase prolactin as a result of dopamine antagonism:
Metoclopramide and Anti-psychotics
109
Sick euthyroid syndrome (non-thyroidal illness) | Levels:
Thyroxine, T3 low usually TSH is normal range in majority of cases No treatment needed.
110
Stress response: Hormones decreased: Hormones which do not change:
Insulin Testosterone Oestrogen TSH, LH, FSH
111
Which hormones increase in stress response:
GH, Cortisol, | Renin, ACTH, Aldosterone, prolactin, ADH, Glucagon
112
Subacute (De Quervains) thyroiditis: presents with: stages:
HYPERthyroidism Phase 1: Hyperthyroid (3-6 weeks) Phase 2: (1-3 weeks) euthyroid Phase 3: Hypothyroid Phase 4: thyroid function and structure back to normal
113
Subacute (De Quervains) thyroiditis on scintigraphy:
Globally REDUCED uptake of iodine-131
114
Subacute (De Quervains) thyroiditis tx.
Usually self-limiting - may respond to aspirin or NSAIDs severe cases: steroids are used esp. if hypothyroid develops
115
Subclinical hyperthyroidism | levels:
Normal thyroxine and T3 | but LOW TSH.
116
Subclinical hyperthyroidism | tx.
Most revert to normal TSH | reasonable to trial low dose antithyroid agents for 6 months to induce remission
117
Subclinical HYPOthyroidism: tx.
TSH high everything else normal Start tx. even if asymptomatic with levothyroxine if <70 y/o In older people (>80yrs) watch and wait.
118
Can SUs be used in pregnancy and breast-feeding
No
119
TZDs | adverse effects:
Wt. gain, liver impairment LFTs Fluid retention - COMPLETE CONTRAINDICATION IN HEART FAILURE Increased risk of FRACTURES Bladder cancer (pioglitazone)
120
Thyroid cancer: | Management of Papillary and follicular:
Total thyroidectomy Followed by radio iodine (I-131) to kill residual cells Yearly THYROGLOBULIN levels
121
Thyroid cancer with Lymphatic spread: Haematogenous spread
Papillary Follicular
122
Calcitonin levels raised in which Thyroid cancer -
Medullary
123
Anaplastic carcinoma: Most common in: Not responsive to:
Elderly | Not responsive to chemotherapy
124
Most modifiable risk factor in development of thyroid eye disease:
Smoking
125
Which thyroid treatment may worsen thyroid eye disease?
Radioiodine ablation
126
Management of thyroid: eye disease
Topical lubricants Steroids Radiotherapy Surgery
127
What therapy is required before starting thyroxine
Steroid therapy
128
What marker of thyroid function is used in TFTs
T4
129
First line investigation for thyroid nodules:
Ultrasound and TFTs
130
Thyroid storm management:
Symptomatic treatment: paracetamol Treat underlying precipitating event Beta-blocker: typically IV propranolol ATDs - PTU or Methimazole Lugol's iodine Dexamethasone (blocks conversion of T4 to T3)
131
Dermatological features of thyrotoxicosis:
``` Thyroid acropachy (clubbing fingers) Pretibial myxoedema (erythema and oedema above the lateral malleoli) Increased sweating ```
132
Toxic multi nodular goitre: Thyroid disturbance: Nuclear scintigraphy Tx. of choice
Hyperthyroidism Patchy uptake Radioiodine therapy
133
Psychogenic polydipsia Starting plasma osmolality: Final urine osmolality: urine osmolality post DDAVP:
Low >400 >400
134
Cranial DI Starting plasma osmolality: Final urine osmolality: urine osmolality post DDAVP:
High <300 >600
135
Nephrogenic DI Starting plasma osmolality: Final urine osmolality: urine osmolality post DDAVP:
High <300 <300