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Medicine > Endo > Flashcards

Endo Flashcards

1
Q

What are the symptoms of hyperprolactinaemia in women?

A

Amenorrhea, galactorrhea, infertility, [compression symptoms]

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2
Q

What are the symptoms of hyperprolactinaemia in men?

A

Hypogonadism, reduced libido, erectile dysfunction, gynaecomastia, galactorrhea [compression symptoms]

Often late presentation: osteoporosis, atherosclerosis - indirect results of hypogonadism)

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3
Q

How do prolactin levels help determine cause of endo pathology?

A

Hypothalamic: prolactin rises
Hypopituitarism: prolactin falls

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4
Q

What is the size of a macroadenoma?

A

> 1cm

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5
Q

What is the most common functioning adenoma?

A

Prolactinoma

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6
Q

How do non-functioning adenomas present?

A

Compression symptoms: headache, vision problems (bitemporal hemianopia or upper temporal quadrantanopia) N+V, cranial nerve palsies

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7
Q

What is Sheehan’s syndrome?

A

Panhypopituitarism following massive obstetric haemorrhage (leading to infarction)

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8
Q

What is pituitary apoplexy?

A

Infarction or haemorrhage of pituitary tumour (eg from HTN or major surgery)

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9
Q

What are the symptoms of pituitary apoplexy?

A

Severe thunder-clap retro-orbital headache, N&V, reduced GCS, ophthalmoplegia + bitemporal hemianopia

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10
Q

What is the principle for testing HYPERpituitarism?

A

Suppression tests (i.e. not suppressed)

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11
Q

What is the principle for testing HYPOpituitarism?

A

Stimulation tests (i.e. not stimulated)

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12
Q

What is the test for excessive growth hormone?

A

Oral GTT (+VE: doesn’t suppress)

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13
Q

What is the test for excessive ACTH or CRH?

A

Dexamethasone (+VE: doesn’t suppress)

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14
Q

What is the test for insufficient GH?

A

Insulin tolerance (+VE: doesn’t stimulate it)

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15
Q

What is the test for insufficient cortisol?

A

Synacthen (ACTH analogue) (+VE: doesn’t stimulate it)

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16
Q

What is the test for insufficient GnRH?

A

Clomifene or LH/FSH (+VE: doesn’t stimulate it)

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17
Q

What are the typical lab findings in diabetes insipidus?

A

Increased plasma osmolality, decreased urine osmolality

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18
Q

What is the test to differentiate between cranial and nephrogenic DI?

A

ADH stimulation:
will correct cranial DI
no effect on nephrogenic DI

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19
Q

What are the typical lab findings in SIADH?

A

Decreased plasma osmolality, increased urine osmolality

Often euvolaemic and normotensive

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20
Q

What is the relationship between dopamine and prolactin?

A

Dopamine inhibits prolactin

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21
Q

What are physiological causes of hyperprolactinaemia?

A

Pregnancy
Puerperium
Breast stimulation
Stress

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22
Q

What are intra-cranial causes of hyperprolactinaemia?

A 
Pituitary tumours
Tumours compressing the pituitary stalk
Head injury
Brain surgery or radiotherapy
Post-ictal
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23
Q

What are endocrine and metabolic causes of hyperprolactinaemia?

A

Hypothyroidism (because increased TRH)
Cushing’s syndrome
Cirrhosis of liver
PCOS

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24
Q

Which drugs cause hyperprolactinaemia?

A

Drugs that block dopamine receptors: domperidone, metoclopramide, neuroleptics, anti-psychotics

Dopamine-depleting agents: methyldopa

Anti-depressants

(+ many more)

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25
Q

What are the initial investigations for hyperprolactinaemia?

A

Exclude pregnancy

Basal serum prolactin (if mildly elevated: repeat, if excessively high: likely prolactinoma)

TFTs

Visual field testing

Assessment of pituitary function

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26
Q

How is a prolactinoma managed first-line?

A

Dopamine agonists: cabergoline, bromocriptine, quinagolide

Usually sufficient to shrink tumour (may need several years)

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27
Q

What are the causes of cranial DI?

A 
Idiopathic
Tumours
Intracranial surgery
Head injury
Granulomata
Cerebral infections
Vascular disorders
Post-radiotherapy
Inherited
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28
Q

What are the causes of nephrogenic DI?

A 
Idiopathic
Hypokalaemia
Hypercalcaemia
CKD
Drugs, eg lithium 
Renal tubular acidosis
Pregnancy
Post-obstructive uropathy
Inherited
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29
Q

Why may DI cause incontinence in those able to get to the toilet?

A

Chronic overdistension of bladder

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30
Q

How may the signs in a pt with DI?

A

Signs of dehydration

Bladder may be enlarged and palpable

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31
Q

What investigations should you carry out in a patient with suspected DI?

A 
24-hour urine collection
Urine specific gravity
Simultaneous plasma and urine osmolality
U&Es
Plasma glucose
Serum calcium

Fluid deprivation test with response to desmopressin

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32
Q

Interpreting causes of DI on basis of water deprivation and desmopressin:

Urine Osmolality:
Before: low - After: high
Before: low - After: low
Before: high - After: high

A
  1. Cranial DI
  2. Nephrogenic DI
  3. Primary/ psychogenic polydipsia
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33
Q

What is the Mx of cranial DI?

A

Desmopressin (monitor for hyponatraemia, have tablet-free days)

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34
Q

What is the Mx of nephrogenic DI?

A

None just allow good access to fluids and correct metabolic abnormalities, drugs etc.

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35
Q

When may serum osmolality be normal (or increased) and urine osmolality be increased?

A

Dehydration, renal disease, congestive heart failure, Addison’s, hypercalcaemia, hyperglycaemia, hypernatraemia, alcohol ingestion, mannitol therapy

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36
Q

When may serum osmolality be normal (or increased) and urine osmolality be decreased?

A

DI

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37
Q

When may serum osmolality be decreased and urine osmolality be increased?

A

SIADH

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38
Q

When may serum osmolality be decreased and urine osmolality be decreased?

A

Overhydration, hyponatraemia, adrenocortical insufficiency

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39
Q

What are the causes of acromegaly?

A

Pituitary adenoma

Rare:
Ectopic GH from tumour
Inherited

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40
Q

Why are those affected with acromegaly susceptible to vertebral fractures?

A

Low-quality bone despite high bone mass

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41
Q

Why is acromegaly not tested with random GH?

A

Secretion is episodic and half-life is short

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42
Q

Which cancers are screened for in acromegaly?

A

Colon

Thyroid

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43
Q

What are the investigations for suspected acromegaly?

A

IGF-1
Assessment of other pituitary hormones as indicated: prolactin, adrenal, thyroid, gonadal

Blood glucose
Bone profile
Serum triglycerides

Visual tests

OGTT to confirm a raised IGF-1

ECG + echo

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44
Q

What is first-line management of acromegaly?

A

Trans-sphenoidal surgery (i.e. adenoma)

Otherwise, somatostatin analogues, eg octreotide

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45
Q

What are the causes of pseudo-acromegaly?

A

Insulin resistance associated with hyperinsulinaemia

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46
Q

What is the name for symptomatic hyperthyroidsm?

A

Thyrotoxicosis

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47
Q

What are the causes of hyperthyroidism? (7)

A 
Graves
Overgrowth of gland
Tumour
Subacute thyroiditis (de Quervain's)
Ectopic thyroid tissue
Over-treatment of hypothyroidism
Drugs: amiodarone, thyroxine OD
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48
Q

What Ix would you carry out following TFTs?

A

Autoantibody screen
?Radioisotope scan (show ‘hot’ areas)
ECG if hyper (sinus tachy, AF)

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49
Q

What are the management options for hyperthyroidism?

A

Carbimazole (1 month for effect, sometimes block-and-replace)
Beta-blockers (palpitations, anxiety)
Radioiodine (slow uptake, may still need carbimazole)
Partial thyroidectomy

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50
Q

What blood finding in Graves?

A

Autoantibodies against TSH receptors

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51
Q

Graves eye disease:

  1. What are the findings?
  2. What is the cause?
  3. Management
A
  1. Exophthalmos, conjunctival oedema, lid lag, proptosis, weakening of extraocular muscles, keratitis (if trouble closing)
  2. Inflammation causes lymphocyte infiltration + activation of fibroblasts secreting osmotically-active hyaluronic acid
  3. STOP SMOKING, prednisoolone, lubricants
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52
Q

What is the name for symptomatic hypothyroidism?

A

Myxoedema

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53
Q

What are the causes of hypothyroidism? (7)

A

Hashimoto’s
Over-treatment of hyperthyroidism
De Quervain’s
Primary atrophic hypothyroidism
Dyshormogenesis (inherited defect, goitre)
Iodine deficiency
Drugs: lithium, amiodarone, excess iodine

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54
Q

How is hypothyroidism treated?

A

Levothyroxine

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55
Q

In emergencies, what medication is given to rectify hypothyroidism?

A

liothyronine (T3)

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56
Q

What are the ADRs of thyroxine?

A

Hyperthyroidism symptoms

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57
Q

What are the ADRs of carbimazole?

A

Hypothyroidism symptoms

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58
Q

In hypopituitarism, what must be corrected first?

A

Corticosteroids first to avoid Addisonian crisis

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59
Q

Which medications reduce absorption of thyroxine?

A

Calcium, iron replacements, antacids

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60
Q

What is the common sequence of symptomology experienced in Hashimoto’s?

A

Hyper –> eu –> hypo

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61
Q

De Quervain’s

  1. Definition
  2. Epidemiology
  3. Symptoms
  4. Pathology
  5. Prognosis
A
  1. Inflammation of gland by virus
  2. Young, middle-age women
  3. Tender, swollen + febrile illness
  4. Inflammation causes destruction of follicles, then immune reaction causes granulomas to form
  5. Usually left with hypo symptoms until gland recovers (days/ months)
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62
Q

Who is commonly affected by primary atrophic hypothyroidism?

A

Elderly - there is atrophy and fibrosis of gland.

Thought to be end-stage of many thyroid diseases

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63
Q

Causes of goitres

A

Physiological: puberty, pregnancy
Hyper: Graves’ (bruits, v vascular), thyroiditis
Hypo: all
Multi-nodular goitre (‘toxic’ if these produce hormones)

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64
Q

What might precipitate a thyroid emergency?

A

Surgery, radioiodine, infection, MI, stroke

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65
Q

What are the symptoms of thyrotoxic crisis (thyroid storm)?

A

Pyrexia, confusion, D+V, life-threatening arrhythmias, coma

66
Q

What are the symptoms of a myxoedema coma?

A

Hypothermia, hyporeflexia, hypoglycaemia, bradycardia, seizures, coma

67
Q

What TFTs would tell they require steroid therapy prior to thyroxine?

A

Secondary hypothyroidism (ie pituitary):
TSH LOW
T4 LOW

68
Q

What TFTs may suggest subclinical hypothyroidism or poor compliance with thyroxine?

A

TSH High

T4 NORMAL

69
Q

What do TFTs show in sick euthyroid syndrome (non-thyroidal illness)?

A 
TSH Low (or normal)
T4 Low (and esp T3)
70
Q

How can steroid therapy affect TFTs?

A

TSH: low
T4: normal

71
Q

What % thyroid lumps are benign?

How should they be investigated?

A

80%

TFTs + fine-needle aspiration

72
Q

What is the mnemonic for thyroid cancers?

A

People forget medicine and mumble

Papillary
Follicular
Medullary
Anaplastic
Malignant lymphoma
73
Q

Which thyroid cancer is associated with ectopic hormone production?

A

Medullary: arise in para-follicular cells
Calcitonin (usually asymptomatic)
ACTH (Cushing’s)
5-HT (Carcinoid syndrome)

74
Q

Describe the histology of the adrenal gland

A

GFR+ MEGA

G- mineralocorticoids
F- glucocorticoids
R- androgens

medulla: 20% NA-secreting / 80% adrenaline-secreting

75
Q 
Mineralocorticoids:
Example
What are they stimulated by? (Which isn't v significant)
Where does it act?
What does it do?
A

Aldosterone
Hyperkalaemia, ACE II and ACTH (not so much)
Acts on DCT/CD
Increases water + salt retention, excretes K+

76
Q

Glucocorticoids:
Example
Function
How does it exert circadian rhythm?

A

Cortisol
Regulates metabolism of carbs + proteins, maintains glucose levels when fasting / potent anti-inflammatory + immmunosuppressant
At 6am, exerts weaker neg feedback on CRH –> ACTH

77
Q

Where are androgens from medulla converted to more active ones - under what enzyme?

A

In peripheral tissues, aromatase

78
Q

When does the cortex start secreting androgens?

A

Andrenarche: 7-9 years

79
Q

What are the signs of hyperaldosteranism?

A 
Water + salt retention > hypertension
[but not hypernatraemia due to other mechanisms]
Polyuria + polydipsia
Hypokalaemia
Alkalosis
Muscle weakness + spasm
80
Q

What are the investigations of hyperaldosteronism?

A

U&Es
aldosterone
renin levels: decreased in primary, increased in secondary (eg in response to renal or heart failure)
ECG

Will need to be off certain meds

81
Q

What is Conn’s syndrome?

A

A cause of secondary hypertension and hyperaldosteronism, caused by adenoma of zona glomerulosa

82
Q

What are the causes of Cushing’s syndrome? (3)

A

Overtreatment with glucocorticoids
Ectopic ACTH production (eg oat-cell carcinomma)
Carcinoma of adrenal cortex

(Latter two: death may occur before development of cushingoid features)

83
Q

What is Cushing’s disease?

A

Pituitary adenoa causing bilateral enlargement of cortex

Same symptoms + pigmented skin

84
Q

Causes of pseudo-cushings

A

Depression, obesity, alcoholism

85
Q

First-line investigation for Cushing’s syndrome

A

24-hour urinary free cortisol (represents 1%) - ideally 3 collections

86
Q

In whom should suspicions of Addison’s be considered?

A

Hx of craving for salty food, postural hypotension, pigmented skin

Addisonian crisis

Unexplained recurrent hypoglycaemia

Hypothyroidism that gets worse despite thyroxine

Other auto-immune disease

87
Q

What investigations should be carried out for adrenal insufficiency?

A

NB may be normal - no reserve when stressed

FBC
U&Es
Calcium
Glucose
LFTs
Cortisol (between 8am-9am when highest)

Followed by:
ACTH
Renin:aldosterone (renin usually high, aldosterone low)
Synacthen test

88
Q

What would be done during Addison’s ongoing monitoring?

Hx
Examination
Ix

A

Questions about symptoms, eg energy + appetite - questions about other auto-immune diseases (thyroid, diabetes, pernicious anaemia, coeliac)

Weight, BP (sitting + standing), examination of skin for pigmentation

U&Es, bone profile, TFTs, glucose + HbA1c, FBC, B12

89
Q

What should be in an emergency Addison kit?

What are the sick days rules?

A

Hydrocortisone self-injection

Double the hydrocortisone

90
Q

What are the typical biochem findings in Addison’s?

A

hyponatraemia, hyperkalaemia, hypoglycaemia, tendency for hypercalcaemia

91
Q

What are causes of acute adrenocortical failure?

How does it present?

A

Bilateral haemorrhagic necrosis (sepsis/ DIC/ Waterhouse-Friderichson syndrome [meningococcal])
Stopping steroids suddenly (steroids stop ACTH production - so no endogenous cortisol for weeks)

92
Q

How are phaechromocytomas treated?

A

Alpha-blockers for ~10 days, then surgery

93
Q

Tumours where can produce same symptoms of phaechromocytomas?

A

Sympathetic ganglion (usually beside aortic bifurcation)

94
Q

Order steroids in terms of mineralocorticoid content…

A

Fludrocortisone
Hydrocortisone (think water)
Prednisolone
Dexamethasone, betmethasone

95
Q

What are the side-effects of steroids?

A

Glucocorticoids (Cushing’s)

Mineralocorticoids (like hyperaldosteronism) - be wary of prescribing alongside other meds that cause hypokalaemia

96
Q

What should you consider prescribing alongside steroids?

A

Steroid-sparing agent, eg azathioprine, methotrexate
Bisphosphonates
PPIs

97
Q

Causes of hyperglycaemia

A

DM

Glucagonoma

98
Q

Causes of hypoglycaemia

A 
Anti-diabetic meds/ poor control
Alcohol
Pituitary insufficiency (reduced GH)
Insulinoma/ ectopic insulin
Drugs: quinine, salicylates, propanolol
99
Q

What is MODY?

A

Maturity-onset Diabetes of the Young

inherited, young patients, often not obese, at risk of DKA

100
Q

What is LADA?

A

Latent Autoimmune Diabetes of Adults

often misdiagnosed as T2DM

101
Q

If a patient is symptomatic for DM, how can this be diagnosed?

A

Fasting: 7+
Random: 11.1+
HbA1C: 6.5% (48 mmol) - but normal does not rule out

102
Q

How is an asymptomatic pt diagnosed with DM?

A

Two readings

103
Q

How is pre-diabetes diagnosed?

A

Fasting: 6.1 - 6.9
HbA1C: 42-47

104
Q

When should HbA1C not be used?

A

When RBC life is prolonged (eg asplenic), or when RBC life is shortened (eg SCD)

Children + gestational

105
Q

What medication is first-line for hypertension in DM?

A

ACEi (renoprotective)

If black, ACEi + thiazide/CCB

106
Q

How is HHS differentiated from DKA?

A

Ketonuria ++ in DKA

107
Q

What are the findings in DKA?

A

Dehydrated (glucose + ketones form diuresis)
Metabolic acidosis (ketones)
Hypokalaemia

108
Q

What are the complications of DKA?

A

Cerebral oedema in kids

Cardiac dysarrhythmias

109
Q

What are the causes of secondary diabetes?

A

Pancreatic disease: cystic fibrosis, chronic pancreatitis, pancreatectomy, ca pancreas

Endocrine: Cushing’s, acromegaly, thyrotoxicosis, phaechromocytoma, glucagonoma

Drugs: CS, among others

Hereditary: Friedrich’s ataxia, haemachromatosis

110
Q

What is ideal BP if DM?

A

135/85

unless signs of end-stage organ damage: 130/80

111
Q

When should short-acting insulin be injected?

A

15-30 mins before meal

112
Q

How often should BM be checked if on insulin?

A

4 times/day (before each meal and before bed)

every 4 hours if ill

113
Q

What level of hypoglycaemia should be treated in hospitals?

114
Q

Less-obvious way for hypoglycaemia to present?

A

Cardiac event

115
Q

How often should HbA1c be checked in T2DM?

A

3-6 monthly until stabilised

6 monthly thereafter

116
Q

What is HbA1c target in T2DM?

A 
48 mmol (6.5%) if on mono-therapy
7.0% if on drugs associated with hypoglycaemia

Consider relaxing on case-by-case basis

117
Q

Symptoms and management of gastroparesis

A

Gastrc bloating and vomiting

Domperidone

118
Q

Side-effects of metformin

A

Lactic acidosis
GI disturbance

Step-up gradually

119
Q

Mechanism of metformin

A

Increase insulin sensitivity

Decrease hepatic gluconeogenesis

120
Q

Mechanism of sulfonylureas

A

Stimulate pancreatic beta cells

121
Q

Side-effects of sulfonylureas

A

Hypoglycaemia

Hyponatraemia

122
Q

Examples of sulfonylureas

A

Gliclazide

Glimepiride

123
Q

What are the sick day rules for diabetics?

A

Keep a sick day pack with sugary food and fluids
Keep eating + drinking
Continue taking meds (inc insulin)

If T1DM: ketone sticks, 4-hourly BMs

If unable to eat and drink properly, seek medical advice

124
Q

Normal serum calcium level

A

2.1 to 2.6

125
Q

Symptoms + signs of hypocalcaemia

A 
Paraesthesia
Muscle cramps
Carpopedal spasm
Chvostek's sign
Trousseau's sign

Seizures
Prolonged QT (leading to VF, heart block)
Laryngospasm
Bronchospasm

126
Q

Causes of hypocalcemia

A 
If low PTH: 
parathyroid agenesis (eg DiGeorge's syndrome)
parathyroid destruction (surgery, radiotherapy, infiltrative disease)
autoimmune disease

If high PTH:
vit D deficiency
hypomagnesaemia
pseudohypoparathyroidsm (PTH resistance)

Other:
hyperventilation
drugs (eg bisphosphonates)
acute pancreatitis
acute rhabdomyolysis
malignancy
127
Q

How to investigate hypocalcaemia?

A

Check: ideally take fasting blood sample fro uncuffed arm, ensure using adjusted calcium

U&Es (exclude CKD)
amylase (exclude acute pancreatitis)
creatinine kinase (exclude rhabdo)
Phosphate
Mg
Vit D

ECG

128
Q

How do you treat acute symptomatic hypocalcaemia?

A

Give 10 mL of calcium gluconate 10% by slow IV injection

Repeat if necessary (up to 40 mL/24h)

(Correct hypomagnesaemia first)

129
Q

Which hypocalcaemics are prescribed calcitriol?

A

Renal impairment: doesn’t require hydroxylation by kidney

130
Q

What are the symptoms of hypercalcaemia?

A

Mild: polyuria, polydipsia, dyspepsia, depression, mild cognitive impairment

Moderate: also muscle weakness, constipation, anorexia, nausea, fatigue

Severe: abdo pain, vomiting, dehydration, shortened QT interval, pancreatitis, coma

If long-standing, calcium deposited in soft tissues + stones

131
Q

What are the causes of hypercalcaemia?

A

PTH-mediated

Malignancy
Granulomatous conditions

Others

132
Q

What investigations for hypercalcaemia?

A

PTH
U&Es
Serum phosphate
ALP

(Consider urine calcium + phosphate)

133
Q

When are PTH levels low in hypercalcaemia?

A

Granulomatous disease, renal dialysis, adrenal insufficiency, thyrotoxicosis

134
Q

How should acute hypercalcaemia be administered?

A

IV fluids
After rehydration, bisphosphonates IV

Sometimes steroids or other drugs, depending on cause

135
Q

Does vit D (calcitriol) increase or decrease serum calcium?

A

Increases absorption from gut

136
Q

Causes of primary hyperparathyroidism

A

PT adenoma (80%), hyperplasia (20%)

137
Q

Causes of secondary hyperparathyroidism

A

chronic renal disease
vit D deficiency/ malabsorption

ie IN RESPONSE TO LOW CALCIUM

138
Q

When may osteitis fibrosa cystica result?

A

Secondary hyperparathyroidism

139
Q

How is secondary hyperparathyroidism managed?

A

Diet modification/ phosphate binders

Vit D analogues

140
Q

What is tertiary hyperparathyroidism?

A

If secondary hyperparathyroidism persists, level of calcium needed resets/ autonomous secretion of PTH

141
Q

What are the lab findings in the three types of hyperparathyroidism?

A

PTH increased always

1: increased calcium, decreased phosphate
2: normal/ decreased calcium, increased phosphate
3: normal/ increased calcium, normal or decreased phosphate, normal or decreased vit D, increased ALP

142
Q

What produces calcitonin?

A

C cells of thyroid

143
Q

What investigations for hyponatraemia?

A 
U&Es
Glucose
Lipids
TFTs
LFTs
Plasma osmolality

Urine osmolality
Urine Na + K

144
Q

What are the causes of hypernatraemia?

A

Pure free water loss, eg poor intake, DI

Hypotonc fluid loss, eg excessive sweating, burns, GI losses, urinary losses (eg diuresis)

Hypertonic sodiu gain, eg iatrogenic

145
Q

What investigations for hypernatraemia?

A

U&Es
Calcium
Plasma glucose

Lithium levels, where appropriate (reduces lithium elimination)

If DI suspected: urine and serum osmolality

146
Q

What is management of hypernatraemia?

A

Address underlying cause, withhold diuretics, lactulose

Seek specialist help so not to correct too rapidly (esp if chronic)
There are formulae to calculate amount of free water needed

147
Q

What are the main causes of hypokalaemia?

A

Diuretics

GI lossses

148
Q

What investigations for hypokalaemia?

A

Check with ABG

ECG: flat t waves, ST depression, prominent U waves

U&Es (concurrent low sodium suggests thiazides or marked volume depletion)
Serum bicarbonate
Serum glucose
Serum chloride
Serum magnesium
Urine: 
osmolality (needed to interpret urine K)
urinary potassium (high = renal loss)
urinary sodium (if low, and urinary K high = secondary hyperaldosteronism)
149
Q

How to manage hypokalaemia?

A

Usually diet/ oral supplements
Administer KCl

Monitor 1-3 hourly

150
Q

What investigations for hyperkalaemia?

A

Check: ABG

FBC
U&Es
Capillary + plasma blood glucose
24h urinary volume and electrolytes

If takes digoxin, check levels

151
Q

What are the ECG changes in hyperkalaemia?

A

Tented t waves
Prolongation of PR interval
Widening of QRS
Other shit

If already has heart disease, bradycardia may be only new thing

152
Q

How to manage hyperkalaemia?

A

If above 7 or ECG changes:

Stop medications that conserve potassium
Consider stopping digoxin and beta-blockers

10 mL 10% calcium gluconate (protect cardiac membrane) - up to 50 mL until ECG stabilises
Effects only last 30-60 mins

Insulin-glucose infusion (usually 10 units/25 g glucose) by IV: check BM before, during + after

Also give 10-20 mg nebulised salbutamol

Are other things to try, haemodialysis if necessary

153
Q

MEN I

A

3 Ps
Parathyroid
Pituitary
Pancreas (insulinoma/ Zollinger-Ellinson)

154
Q

MEN IIa

A

2 Ps
Medullary thyroid cancer
Parathyroid
Phaechromocytoma (bilateral)

155
Q

MEN IIb

A

1 P
Medullary thyroid cancer
Phaechromocytoma
(Marfanoid body, neuromas)

156
Q

PLACEHOLDER

A

Diabetes Meds

157
Q

Endo causes of clubbing

A

Thyroid acropachy

158
Q

Main steps in medical management of T2DM

A

Diet alone/ metformin: 48 mmol (6.5%)

Meds that might cause hypo, eg sulphonylurea: 53 mmol (7%)

If rises to 58 mmol (7.5%) - intensify treatment - add insulin (+metformin, +sulphonylurea)

159
Q

Pregnancy and hyperthyroidism precaution

A

Carbimazole and methimazole are teratogenic

Propylthiouracil used instead

160
Q

Thyroid and periods

A

Hyper: amenorrhea
Hypo: menorrhagia

161
Q

What produces a woody hard thyroid?

A

Riedel thyroiditis
typically euthyroid but can be hypothyroid due to autoimmune fibrosis
can cause compression of local structures
treat with pred

162
Q

which common med reduces hypoglycaemic awareness

A

beta-blockers

Medicine (30 decks)

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