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Human Development > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Adrenal insufficiency/Addison’s definition

A

Adrenal glands do not produce enough steroid hormones (cortisol & aldosterone)

Addison’s disease = primary adrenal insuff. caused by autoimmunity

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2
Q

Primary adrenal insufficiency definition

A

Adrenal glands damaged, resulting in low cortisol and aldosterone secretion (inc. Addison’s; specifically autoimmune)

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3
Q

Secondary adrenal insufficiency definition

A

Inadequate ACTH resulting in a lack of stimulation of adrenal glands

Result of loss of/damage to pituitary from pituitary adenoma, surgery, radiotherapy or trauma

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4
Q

Tertiary adrenal insufficiency definition

A

Insufficient CRH release from hypothalamus

Usually from patients on long-term (>3 weeks) steroids not tapering doses correctly

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5
Q

Adrenal insufficiency presentation

A

Fatigue
Muscle weakness
Muscle cramps
Dizziness and fainting
Thirst and craving salt
Weight loss
Abdominal pain
Depression
Reduced libido

Bronze hyperpigmentation of the skin, particularly in creases (ACTH stimulates melanocytes to produce melanin)
Hypotension (particularly postural hypotension – with a drop of more than 20 mmHg on standing)

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6
Q

Adrenal insufficiency investigations

A

Hyperkalaemia (high potassium)
Hypoglycaemia (low glucose)
Raised creatinine and urea due to dehydration
Hypercalcaemia (high calcium)

Early morning cortisol often falsely low

ACTH measured directly may be high or low depending on primary/secondary/tertiary

Adrenal cortex or 21-hydroxylase antibodies may be present in Addison’s

CT or MRI of adrenal glands or MRI of pituitary may be helpful

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7
Q

Test for adrenal insufficiency

A

Short synacthen test

Synthetic ACTH given & cortisol checked after 30 and 60 minutes

Should double cortisol levels

If failure to double, either primary adrenal insufficiency or significant adrenal atrophy from prolonged secondary adrenal insufficiency

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8
Q

Management of adrenal insufficiency

A

Hydrocortisone to replace cortisol

Fludrocortisone to replace aldosterone if needed

When ill, double hydrocortisone dose to mimic body’s response to stressors, and attend A&E if vomiting

Will have medical ID bracelet and steroid card, and should carry emergency hydrocortisone injection

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9
Q

Adrenal crisis definition, presentation & management

A

Acute presentation of severe adrenal insufficiency

Present with:
Reduced consciousness
Hypotension
Hypoglycaemia
Hyponatraemia and hyperkalaemia

Manage with IV hydrocortisone, IV fluids, IV dextrose
ABCDE approach to management

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10
Q

Hyperthyroidism definition

A

Over-production of thyroid hormones, T3 & T4 by thyroid gland

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11
Q

Thyrotoxicosis definition

A

Effects of an abnormal/excessive amount of thyroid hormones on the body

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12
Q

Primary hyperthyroidism definition

A

Dysfunction of the thyroid gland itself, producing excessive thyroid hormone e.g. Grave’s disease, in which autoantibodies stimulate TSH receptors

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13
Q

Secondary hyperthyroidism definition

A

Dysfunction of the pituitary or hypothalamus and over-production of TSH e.g. from a pituitary adenoma

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14
Q

Sub-clinical hyperthyroidism definition

A

Thyroid hormones (T3/T4) are normal but TSH is suppressed/low

(May have mild or absent symptoms)

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15
Q

Grave’s disease definition

A

Form of primary hyperthyroidism in which anti-TSH receptor antibodies bind to the receptors on the thyroid and stimulate excessive thyroid hormone secretion

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16
Q

Plummer’s disease definition

A

Form of primary hyperthyroidism in which nodules develop on the thyroid gland which are unregulated by the thyroid axis and continually secrete thyroid hormones

(Most common in patients >50 years old)

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17
Q

Grave’s disease presentation

A

In addition to the universal symptoms of hyperthyroidism
Also present with Grave’s eye disease, which is evident via lid lag and exophthamos
Pretibial myxoedema (gives skin a discoloured, waxy, oedematous appearance)
Goitre

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18
Q

Hyperthyroidism presentation

A

Anxiety and irritability
Sweating and heat intolerance
Tachycardia
Weight loss
Fatigue
Insomnia
Frequent loose stools
Sexual dysfunction
Brisk reflexes on examination

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19
Q

Thyroid storm presentation and management

A

Acute presentation of hyperthyroidism

Presents with fever, tachycardia and delirium

symptomatic treatment e.g. paracetamol
treatment of underlying precipitating event
beta-blockers: typically IV propranolol
anti-thyroid drugs: e.g. methimazole or propylthiouracil
Lugol’s iodine
dexamethasone/hydrocortisone - blocks the conversion of T4 to T3

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20
Q

Hyperthyroidism management & drug contraindications

A

Carbimazole = first line drug
Propylthiuracil = second line drug

(Both can cause agranulocytosis, if suffering sore throat stop taking and see a doctor ASAP

Carbimazole is contraindicated in pregnancy)

Propranolol for symptomatic relief

Radioactive iodine can be used as a definitive treatment

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21
Q

Hyperparathyroidism definition

A

Overactivity of the 4 parathyroid glands, resulting in excessive secretion of PTH

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22
Q

Hyperparathyroidism presentation

A

Bones, moans, stones & groans

(bone pain, depression, delirium, kidney stones, abdominal moans [vomiting, nausea and constipation])

Categorised by hypercalcaemia

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23
Q

Primary hyperparathyroidism definition, biochem presentation and management

A

Uncontrolled PTH release from the parathyroid glands e.g. from a tumour

Presents with elevated PTH and calcium

Manage surgically

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24
Q

Secondary hyperparathyroidism definition, biochem presentation and management

A

Insufficient vitamin D or chronic kidney disease reduces calcium absorption, leading to hypocalcaemia

Presents with elevated PTH but low/normal calcium

Treat by correcting underlying condition

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25
Q

Tertiary hyperparathyroidism definition, biochem presentation and management

A

Caused by hyperplasia of the parathyroid gland due to prolonged secondary hyperparathyroidism post-resolution

Presents with high PTH and high calcium

Treat by surgically removing part of parathyroid tissue

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26
Q

Hypothyroidism definition

A

Insufficient thyroid hormones, T3 & T4

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27
Q

Primary hypothyroidism definition & biochem

A

Thyroid behaves abnormally and produces inadequate thyroid hormones e.g. iodine deficiency

Loss of negative feedback, hence presents with elevated TSH

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28
Q

Secondary hypothyroidism definition & biochem

A

Secondary hypothyroidism is often associated with a lack of other pituitary hormones, such as ACTH, referred to as hypopituitarism. This is rarer than primary hypothyroidism, and may be caused by:
Tumours (e.g., pituitary adenomas)
Surgery to the pituitary
Radiotherapy
Sheehan’s syndrome (where major post-partum haemorrhage causes avascular necrosis of the pituitary gland)
Trauma

Low TSH, Low T3/4

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29
Q

Hashimoto’s thyroiditis definition

A

Autoimmune condition associated with anti-TPO and anti-Tg

Causes goitre followed by wasting/atrophy of thyroid gland

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30
Q

Hypothyroidism management

A

Oral levothyroxine = first-line treatment (synthetic T4)
Liothyronine sodium = rarely used under specialist care (synthetic T3)

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31
Q

Hypothyroidism presentation

A

Weight gain
Fatigue
Dry skin
Coarse hair and hair loss
Fluid retention (including oedema, pleural effusions and ascites)
Heavy or irregular periods
Constipation
Goitre for iodine deficiency

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32
Q

Cushing’s syndrome & disease definition

A

Refers to prolonged high levels of glucocorticoids in the body (primarily cortisol)

Cushing’s disease refers specifically to high levels from a pituitary adenoma secreting excessive ACTH

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33
Q

Cushing’s syndrome presentation

A

Round face (known as a “moon face”)
Central obesity
Abdominal striae (stretch marks)
Enlarged fat pad on the upper back (known as a “buffalo hump”)
Proximal limb muscle wasting (with difficulty standing from a sitting position without using their arms)
Male pattern facial hair in women (hirsutism)
Easy bruising and poor skin healing
Hyperpigmentation of the skin in patients with Cushing’s disease

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34
Q

Causes of Cushing’s mnemonic

A

CAPE

Cushing’s disease
Adrenal adenoma
Paraneoplastic syndrome (ACTH from tumour somewhere other than pituitary)
Exogenous steroids

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35
Q

Cushing’s syndrome diagnostic test

A

Dexamethasone suppression test

First line = low dose overnight test, give dexamethasone at 11pm and check cortisol at 9am - suppressed normally

For the low-dose 48-hour test, dexamethasone (0.5mg) is taken every 6 hours for 8 doses, starting at 9 am on the first day. Cortisol is checked at 9 am on day 1 (before the first dose) and 9 am on day 3 (after the last dose). A normal result is that the cortisol level on day 3 is suppressed. Failure of the dexamethasone to suppress the day 3 cortisol could indicate Cushing’s syndrome, and further assessment is required.

The high-dose 48-hour test is carried out the same way as the low-dose test, other than using 2mg per dose (rather than 0.5mg). This higher dose is enough to suppress the cortisol in Cushing’s syndrome caused by a pituitary adenoma (Cushing’s disease), but not when it is caused by an adrenal adenoma or ectopic ACTH.

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36
Q

Cushing’s syndrome management

A

Trans-sphenoidal (through the nose) removal of pituitary adenoma
Surgical removal of adrenal tumour
Surgical removal of the tumour producing ectopic ACTH (e.g., small cell lung cancer), if possible

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37
Q

Hyperaldosteronism/Conn’s syndrome definition

A

Refers to high levels of aldosterone

Conn’s specifically refers to an adrenal adenoma producing too much aldosterone

May be present in 5-10% patients with hypertension

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38
Q

Primary hyperaldosteronism definition and causes

A

Adrenal glands directly responsible for producing too much aldosterone

Serum renin will be low due to negative feedback

May be due to a bilateral adrenal hyperplasia, adrenal adenoma (aka Conn’s) or familial

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39
Q

Secondary hyperaldosteronism definition and causes

A

Caused by excessive renin stimulating the release of excessive aldosterone

Usually due to disproportionately lower blood pressure in the kidneys e.g. renal artery stenosis, liver cirrhosis, heart failure

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40
Q

Hyperaldosteronism biochem & investigatons

A

High aldosterone
Low renin (primary) or high renin (secondary)
Hypertension
Hypokalaemia
Alkalosis

Adrenal vein sampling
CT/MRI

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41
Q

Hyperaldosteronism management

A

Aldosterone antagonists - eplerenone & spironolactone

Treating underlying cause e.g. surgical removal of tumour

42
Q

Acromegaly definition

A

Result of excessive growth hormone

Usually from pituitary adenoma

Also linked to carpal tunnel syndrome

43
Q

Acromegaly presentation

A

Headaches
Bitemporal hemianopia

Prominent forehead and brow (frontal bossing)
Coarse, sweaty skin
Large nose
Large tongue (macroglossia)
Large hands and feet
Large protruding jaw (prognathism)

44
Q

Acromegaly investigations

A

Insulin-like growth factor-1 can be tested on a blood sample

Also glucose tolerance test

Pituitary MRI

45
Q

Acromegaly management

A

Trans-sphenoidal surgery

Pegvisomant (growth hormone receptor antagonist given daily by a subcutaneous injection)
Somatostatin analogues (e.g., octreotide) block growth hormone release
Dopamine agonists (e.g., bromocriptine) block growth hormone release

46
Q

Phaeochromocytoma definition

A

Tumour of the adrenal glands secreting unregulated and excessive amounts of catecholamines i.e. adrenaline

47
Q

10% rule of phaeochromocytoma

A

10% bilateral
10% cancerous
10% outside adrenal gland

48
Q

Phaeochromocytoma presentation

A

Anxiety
Sweating
Headache
Tremor
Palpitations
Hypertension
Tachycardia

49
Q

Phaeochromocytoma diagnosis

A

Tests include plasma free metanephrines (breakdown products of catecholamines) & 24 hour urine catecholamines

50
Q

Phaeochromocytoma management

A

Alpha blockers e.g. henoxybenzamine or doxazosin
Beta blockers, only when established on alpha blockers
Surgical removal of the tumour

51
Q

Diabetes insipidus definition

A

Rare disease in which the body makes too much urine

Can be cranial DI (lack of ADH) or nephrogenic DI (lack of response to ADH)

52
Q

ADH function

A

Produced in hypothalamus & secreted by posterior pituitary gland

Stimulates water reabsorption from the collecting ducts in the kidneys

Lack of ADH results in polyuria and polydipsia

53
Q

Primary polydipsia definition

A

Primary polydipsia is when the patient has a normally functioning ADH system but drinks excessive amounts of water, leading to excessive urine production (polyuria) - this is not diabetes insipidus

54
Q

Nephrogenic diabetes insipidus definition and causes

A

Collecting ducts of the kidneys do not respond to ADH

Idiopathic
Medications e.g. lithium
Familial (X-linked recessive inheritance for ADH rec gene)
Hypercalcaemia
Hypokalaemia
Kidney diseases

55
Q

Cranial diabetes insipidus definition and causes

A

Hypothalamus does not produce ADH for the pituitary gland to secrete

Idiopathic
Brain tumours
Brain injury
Brain surgery
Brain infection
Familial (ADH gene autosomal dominant inheritance)
Wolfram syndrome

56
Q

Diabetes insipidus presentation

A

Polyuria
Polydipsia
Dehydration
Postural hypotension

57
Q

Diabetes insipidus investigations results

A

Low urine osmolarity
High/normal serum osmolarity
>3l on 24-hr urine collection

58
Q

Diabetes insipidus test

A

Water deprivation test/desmopressin stimulation test

Patient avoids fluids for ~8hrs before test
After water deprivation, urine osmolarity is measured. If low, synthetic ADH (desmopressin) is given, then urine osmolarity is measured over 2-4 hours after

If high urine osmolarity after water deprivation - likely to be primary polydipsia & no ADH is given

Cranial diabetes insipidus - patient lacks ADH, therefore after synthetic ADH given their osmolarity should increase and be high

Nephrogenic diabetes insipidus - ADH will not have an effect therefore osmolarity will still be low

59
Q

Diabetes insipidus management

A

Treat underlying cause

Desmopressin for cranial DI, but monitor sodium for hyponatraemia

Nephrogenic DI can be treated with thiazide diuretics, high dose desmopressin, NSAIDs and good access to water

60
Q

Type 1 diabetes

A

Pancreas no longer able to produce adequate insulin, resulting in a loss of ability to absorb glucose from the blood

61
Q

Type 1 diabetes presentation

A

Polyuria
Polydipsia
Weight loss

(DKA)

62
Q

DKA definition

A

Diabetic ketoacidosis is a consequence of inadequate insulin

When body recognises low glucose due to lack of insulin signalling, ketogenesis occurs, producing ketones. Usually buffered by the kidneys to prevent ketone acids causing acidosis. But when diabetes causes excess ketones, causes life-threatening metabolic acidosis = DKA

63
Q

DKA presentation & usual patients

A

The initial presentation of type 1 diabetes
An existing type 1 diabetic who is unwell for another reason, often with an infection
An existing type 1 diabetic who is not adhering to their insulin regime

Ketoacidosis
Dehydration
Potassium imbalance
Metabolic acidosis w low bicarb
Hyperglycaemia
Sweet smelling breath
Hypotension
Altered consciousness

64
Q

DKA management

A

FIG-PICK
Fluids - normal saline, 1L in first hr then 1L per 2hrs
Insulin - fixed rate infusion
Glucose - if blood glucose <14mmol/L

Potassium
Infection - treat underlying infection if applicable
Chart fluid balance
Ketones - monitor

65
Q

Key complications from DKA treatment

A

Hypoglycaemia (low blood sugar)
Hypokalaemia (low potassium)
Cerebral oedema, particularly in children
Pulmonary oedema secondary to fluid overload or acute respiratory distress syndrome

66
Q

Autoantibodies in T1D

A

Anti-islet cell antibodies
Anti-GAD antibodies
Anti-insulin antibodies

Serum C-peptide can give a measure of insulin

67
Q

Long term T1D management

A

Subcutaneous insulin (rotate injection sites to avoid lipodystrophy)
Monitor carb intake
Monitor blood sugar
Monitor for complications

68
Q

T1D basal-bolus regime

A

Combination of background long-acting insulin injected once a day & short actin insulin injected 30 mins before carb intake

69
Q

Insulin pump definition, pros & cons

A

Small device continuously infusing insulin at different rates to control blood sugar levels
Cannula replaced every 2-3 days and insertion site rotated

Pros:
Better blood sugar control
More flexibility with eating
Fewer injections

Cons:
Difficulties learning to use the pump
Having it attached at all times
Blockages in the infusion set
A small risk of infection

70
Q

T2D risk factors

A

Non-modifiable:

Older age
Ethnicity (Black African/Caribbean & South Asian)
Family history

Modifiable:

Obesity
Sedentary lifestyle
High carb diet

71
Q

T2D presentation

A

Tiredness
Polyuria
Polydipsia
Unintentional weight loss
Opportunistic infection
Slow wound healing
Glycosuria
Acanthosis nigricans

HbA1c >48mmol/mol indicates T2D, repeated 1 month apart to confirm

72
Q

Pre-diabetes definition & criteria

A

Pre-diabetes is an indication that the patient is heading towards diabetes. They do not fit the full diagnostic criteria but should be educated about the risk of diabetes and lifestyle changes

An HbA1c of 42 – 47 mmol/L indicates pre-diabetes

73
Q

T2D management

A

Education
Low-glycaemic index, high fibre diet
Exercise
Weight loss
Anti-diabetic drugs
Monitor/manage complications

74
Q

T2D treatment targets

A

HbA1c

48 mmol/mol for new type 2 diabetics
53 mmol/mol for patients requiring more than one antidiabetic medication

75
Q

T2D medical management

A

First line = metformin
Add SGLT-2 inhibitor if patient has CVD or heart failure or with QRISK >10% (side effect to be aware of = DKA)

Second-line is to add a sulfonylurea, pioglitazone, DPP-4 inhibitor or SGLT-2 inhibitor.

Third-line options are:

Triple therapy with metformin and two of the second-line drugs
Insulin therapy (initiated by the specialist diabetic nurses)

76
Q

Metformin mechanism of action & side effects

A

Increases insulin sensitivity & decreases glucose production by liver

GI symptoms, including pain, nausea, diarrhoea
Lactic acidosis

Try modified-release metformin if bad GI effects

77
Q

SGLT-2 inhibitors mechanism of action & side effects

A

End with suffix -gliflozin

Inhibits sodium-glucose co-transporter 2 protein, preventing reabsorption of glucose from urine

Glycosuria
Increased urine frequency and output
Genital and urinary tract infections (e.g. thrush)
Weight loss
DKA (with moderately raised glucose)
Fournier’s gangrene (rare, severe infection of genitals or perineum)

78
Q

Pioglitazone mechanism of action & side effects

A

Increases insulin sensitivity and decreases liver production of glucose

Weight gain
heart failure
Small increased risk of bladder cancer
Increased risk of bone fractures

79
Q

T2D complications

A

Infections
Diabetic retinopathy
Peripheral neuropathy
Autonomic neuropathy
Chronic kidney disease
Diabetic foot
Gastroparesis
Hyperosmolar hyperglycaemic state

80
Q

T2D neuropathic pain management

A

Amitriptyline – a tricyclic antidepressant
Duloxetine – an SNRI antidepressant
Gabapentin – an anticonvulsant
Pregabalin – an anticonvulsant

81
Q

Hyperosmolar hyperglycaemic state definition, presentation & management

A

Characterised by hyperosmolality (water loss leads to very concentrated blood), hyperglycaemia and the absence of ketones, distinguishing it from ketoacidosis

Presents with polyuria, polydipsia, weight loss, dehydration, tachycardia, hypotension and confusion

Manage with IV fluids and careful monitoring (involve seniors)

82
Q

Hypoglycaemia definition

A

Blood glucose below 3.5 mmol/L

83
Q

Hypoglycaemia presentation

A

Trembling
Sweating
Palpitations
Hunger
Headache
Double vision
Difficulty concentrating
Slurred speech
Confusion
Coma

84
Q

Hypoglycaemia causes

A

Drugs (insulin, sulphonylureas, GLP-1 analogues, DPP-4 inhibitors, beta blockers)
Alcohol
Acute liver failure
Sepsis
Adrenal insufficiency
Insulinoma
Glycogen storage disease

85
Q

Mild hypoglycaemia management

A

ABCDE approach
15-20g of fast-acting carbohydrate
Follow with slow-acting carbohydrate

86
Q

Severe hypoglycaemia management

A

ABCDE approach
200ml 10% dextrose IV
1mg glucagon IM if no IV access (won’t work if alcohol ingestion is cause)
Manage seizures

87
Q

Hypoglycaemia investigations

A

Whipple’s triad:

Plasma hypoglycaemia
Symptoms attributable to a low blood sugar
Resolution of symptoms when correcting blood sugar

Measure insulin, C-peptide and proinsulin levels to differentiate between exogenous and endogenous insulin sources
High C-peptide/proinsulin = endogenous
Low C-peptide/proinsulin = exogenous
Review medication history for drugs that may cause issue

88
Q

Diabetic neuropathy definition

A

Refers to a variety of peripheral nerve disorders as a result of diabetes
Primary causative factor is chronic hyperglycaemia
Develops from both type 1 & type 2 DM

89
Q

Diabetic neuropathy types and presentation

A

Distal Symmetrical Sensory Neuropathy
Most common form
Resulting from loss of large sensory fibres
Sensory loss in a ‘glove and stocking’ distribution, typically affecting touch, vibration and proprioception

Small-fibre Predominant Neuropathy
Due to loss of small sensory fibres
Deficits in pain and temperature sensation in a ‘glove and stocking’ distribution, with episodes of burning pain

Diabetic Amyotrophy
Originates from inflammation of the lumbosacral plexus or cervical plexus
Severe pain around the thighs and hips, along with proximal weakness.

Mononeuritis Multiplex
Typically painful
Defined as neuropathies involving two or more distinct peripheral nerves

Autonomic Neuropathy
Postural hypotension
Gastroparesis
Constipation
Urinary retention
Arrhythmias
Erectile dysfunction

90
Q

Diabetic neuropathy investigations

A

Neuro exam
Nerve conduction studies
Bloods - glucose levels, HbA1c, B12, thyroid function, liver function

91
Q

Diabetic neuropathy management

A

Control blood glucose
Pain control
Manage complications

92
Q

Chvostek’s sign

A

Facial twitch obtained by tapping the distribution of the facial nerve in front of the tragus

Caused by mechanical irritability of peripheral nerves

Indicative of hypocalcemia and is the most reliable test for hypocalcemia

93
Q

Hyperprolactinaemia definition and levels

A

Elevated serum prolactin

Mildly increased levels (400-600mu/L) may be physiological and asymptomatic, higher levels usually pathological

Very elevated levels (>5,000 mu/L) usually imply a prolactin-secreting pituitary tumour

94
Q

Hyperprolactinaemia presentation

A

Amenorrhoea, oligomenorrhoea or anovulatory cycles
Galactorrhoea
Breast pain & enlargement
Infertility
Loss of libido
Hirsutism

For men:
Impotence
Loss of libido
Decreased seminal volume
Galactorrhoea
Gynaecomastia

95
Q

Hyperprolactinaemia investigations

A

MRI/CT
Formal assessment of visual fields

96
Q

Hypercalcaemia secondary to malignancy presentation

A

Hypercalcaemia
Low PTH
Low phosphate
High PTHrP

97
Q

Changes to hypothyroidism medication during pregnancy

A

increase dose by up to 50% in first 4-6 weeks of pregnancy

98
Q

DM1 sick day rules

A

If on insulin, they must not stop it due to the risk of diabetic ketoacidosis
Check blood glucose more frequently, for example, every 1–2 hours including through the night
Consider checking blood or urine ketone levels regularly
Maintain normal meal pattern if possible
If appetite is reduced meals could be replaced with carbohydrate-containing drinks (such as milk, milkshakes, fruit juices, and sugary drinks)
Aim to drink at least 3 L of fluid (5 pints) a day to prevent dehydration

99
Q

DM2 sick day rules

A

Advise the patient to temporarily stop some oral hypoglycaemics during an acute illness
Medication may be restarted once the person is feeling better and eating and drinking for 24-48 hours

Metformin: stop treatment if there is a risk of dehydration, to reduce the risk of lactic acidosis
Sulfonylureas: may increase the risk of hypoglycaemia
SGLT-2 inhibitors: check for ketones and stop treatment if acutely unwell and/or at risk of dehydration, due to the risk of euglycaemic DKA
GLP-1 receptor agonists: stop treatment if there is a risk of dehydration, to reduce the risk of AKI
if on insulin therapy, do not stop treatment, as above
monitor blood glucose more frequently as necessary

100
Q

De Quervain’s thyroiditis

A

Also known as subacute thyroiditis
Hyperthyroid period followed by hypothyroidism, before returning to euthyroid
Can present with antibodies
Results in decreased isotope uptake
Goitre is usually painful

101
Q

Addison’s steroid dosing/regime

A

the hydrocortisone dose is split with the majority given in the first half of the day

102
Q

How many times a day should a type 1 diabetic check blood sugars?

A

At least 4 times a day, including before meals and before bed

Human Development (4 decks)

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