Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

4TH YEAR - CSIM2 > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What are the 5 classes of hormone? Give 2 examples of each.

A
  1. Amino acid derivatives e.g. dopamine, catecholamines 2. Small neuropeptides eg. GnRh, TRH, ADH 3. Large proteins eg. insulin, PTH 4. Steroid hormones eg. cortisol, oestrogen 5. Vitamin derivatives eg. vitamin A,D
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the functions of hormones?

A

Growth Maintenance of homeostasis Reproduction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the difference between primary and secondary endocrine disease?

A

Primary - target organ dysfunction Secondary - pituitary dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

In what zone are mineralocorticoids produced?

A

Zona glomerulosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

In what zone are glucocorticoids produced?

A

Zona fasciculata

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

In what zone are androgens produced?

A

Zona reticularis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What does the adrenal medulla produce?

A

Epinephrine, norepinephrine and dopamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

TSH stimulates the thyroid to produce…

A

T3 - potent T4 - converted to T3 at certain tissue sites (by deiodinisation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

LH stimulates the leydig cells to produce…

A

Testosterone (95% produced in tested, other 5% in adrenal)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

LH stimulates production of…

A

Progesterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

FSH stimulates production of…

A

Oestrogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the roles of progesterone?

A
  • Maintenance of uterine lining - Decreased contractility of uterine smooth muscle - Skin elasticity and bone strength
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the roles of oestrogen?

A
  • Secondary sex characteristics - Inhibition of bone resorption - Altered lipid profile - Vascular endothelium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the pathology of congenital adrenal hyperplasia?

A

21 hydroxylase deficiency resulting in reduced or absent production of cortisol and aldosterone. This means that the androgen pathway, which is unaffected, is favoured.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the symptoms of congenital adrenal hyperplasia?

A

Presents with ambiguous genitalia, hyponatremia, and arrhythmias, soon after birth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the definition of hyponatremia?

A

Sodium < 135 mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the symptoms and signs of hyponatraemia?

A

Symptoms: none, lethargy, cramps, headache, N&V Signs: disorientation, cerebral oedema, seizures, death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the categories of causes of hyponatraemia?

A
  • Pseudohyponatremia
  • Sodium depletion
  • Excess water intake
  • Reduced renal free water clearance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What causes pseudohyponatremia?

A

Hyperglycaemia Hypertriglyceridaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What causes sodium depletion?

A

Renal loss - diuretics, salt wasting, nephropathy, hypoadrenalism

Non-renal - gut loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What causes excess water intake?

A

Diabetes insipidus IV fluids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What causes reduced renal free water clearance?

A

Hypovolaemia - sepsis, portal HTN, renal failure, hypoalbuminaemia

Cardiac failure

Nephrotic syndrome

Hypothyroid

SIAD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How is hyponatremia treated?

A

Give hypertonic saline

Restrict fluid intake - this is because hyponatremia will mean there will be more water and cells will swell.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the pathology of SIADH?

A

Syndrome of Inappropriate ADH Inappropriate continued secretion of ADH from the posterior pituitary or ectopic. Symptoms of hyponatremia!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How is SIADH diagnosed?

A

Hyponatraemia < 135mmol/L

Urine Na > 20mmol/L

Urine osmol >100mOsm/kg

in absence of

  • adrenal failure
  • oedema
  • hypotension
  • non-osmotic ADH release

Plasma osmol < 280mOsm/kg

Also renal AQP2 excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What causes SIADH?

A

Brain damage (meningitis/SAH) Malignancy (SCLC) Drugs (carbamazepine, SSRIs, amitriptylline) Infection (pneumonia) Hypothyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How should SIADH be managed?

A

Fluid restriction

Sodium replacement SLOW

Treatment of underlying cause

NB - patients can tolerate chronic low sodium but the correction needs to be slow or the patient is at risk of osmotic demyelination syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is osmotic demyelination syndrome?

A

Severe damage and necrosis of the myelin sheath from rapid correction of hyponatremia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the symptoms of osmotic demyelination syndrome?

A
  • Quadriplegia - Opthalomoplegia - Pseudobulbar palsy - Coma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

How can osmotic demyelination syndrome be prevented?

A

Dont let sodium rise more than 10mmol/L/24h

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

A patient has hyponatremia with urine >100mOsmol/kg and urine >30mmol Na What are your differentials?

A

Drugs (ACEis diuretics) SIAD Salt wasting nephropathy Hypoadrenalism Vomiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

A patient has hyponatremia with urine >100mOsmol/kg and urine <30mmol Na What are your differentials?

A

Low arterial volume Heart failure Cirrhosis Nephrotic syndrome Hypoalbuminaemia Third space loss GI loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the definition of hypernatremia?

A

>144 Na

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What are the symptoms and signs of hypernatremia?

A

Symptoms: THIRST, confusion, weakness, appetite loss, nausea Signs - muscle twitching, spasms, seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What causes hypernatremia?

A

Excess sodium in IV therapy Dehydration (elderly, terminally ill)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the management of hypernatremia?

A

Hypotonic fluids IV If hyper<24 hrs - rapidly If hyper >48 hr - slowly Hypotonic means that fluid will move into the cells along a concentration gradient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is the definition of hypokalemia?

A

<3.5 potassium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are the symptoms and signs of hypokalemia?

A

Symptoms: ASYMPTOMATIC, constipation, fatigue, weakness/neuromuscular, cramps, palps Signs: ARRHYTHMIA on ECG, paralysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What causes hypokalemia?

A

Diuretics Conns syndrome Barrters syndrome Gitelmans syndrome Diarrhoea/laxative use

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are the complications of hypokalemia?

A

Cardio -arrhythmias

Neuromuscular - tetany, paralysis, rhabdomyolysis

Renal - decreased GFR, nephritis, metabolic alkalosis

Endocrine - growth retardation, decreased insulin secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is the definition of hyperkalemia and what causes it?

A

>5 potassium

Decreased excretion - renal failure, drugs, hypoaldosteronism, acidosis

Increased release from cell - acidosis, tissue damage, digoxin, vigorous exercise

Increased extraneous load - potassium chloride, blood transfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What are the symptoms and signs of hyperkalemia?

A

Symptoms: Parasthesia, weakness Signs: ARRHYTHMIA, paralysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What are the complications of hyperkalemia?

A

Cardio - arrhythmias Neuromuscular - parasthesia, weakness Renal - decreased renal NH4 production Endocrine - increased insulin secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

How is hyperkalemia managed? (think rule of 10s)

A
  1. IV calcium gluconate 10% 10mg
  2. IV actrapid (10units) and dextrose (25g)
  3. IV saline 50ml
  4. Salbutamol neb 10-20mg

Stop potassium containing/sparing meds. Dialysis if no response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is given to stabilise the membrane in hyperkalemia ?

A

IV calcium gluconate 10% 10ml over 10 min IV saline 50ml

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is given to push potassium back into the cells in hyperkalemia?

A

Salbutamol 10-20mg nebulised IV actrapid 10units (and IV dextrose 25g to prevent hypoglycaemia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What are the ECG features of hypokalemia?

A
  • ST depression - Flat T wave - Prominent U wave
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What are the ECG features of hyperkalemia?

A

Tented T waves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Where is potassium primarily stored?

A

Muscles, liver, RBCs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Where is the main place of potassium reabsorption in the kidney?

A

Proximal convoluted tubule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

How is hypokalemia treated?

A

Sando potassium tablets

Mild (3-4) - TDS

Moderate (2.5-2.9)- QDS

Severe (<2.5) - IV 40mmol KCL in 1L saline (1mmol/hr)

If IV, give in central line as K irritates tissues

Dont give bolus as risk of arrhythmia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What is Barrters syndrome?

A

A range of inherited defects in the loop of hence in TAL Na+ and Cl- transport that causes hypokalemia and metabolic alkalosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What is Gitelmans syndrome?

A

An inherited thiazide-like defect in DCT Na+/Cl- transport that causes hypokalaemia and metabolic alkalosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What hormones does the anterior pituitary produce?

A

ACTH TSH FSH/LH Prolactin GH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What hormones does the posterior pituitary produce?

A

ADH (vasopressin) Oxytocin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

In general, what causes pituitary hormone deficiency?

A

Congenital Acquired - SOL - Trauma - Iatrogenic - Infection - Infiltrative/inflam disease - Vascular - Idiopathic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

In general what causes pituitary hormone excess?

A
  • Benign pituitary adenoma - Ectopic secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What are ‘mass effect’ symptoms when referring to pituitary disease, and what causes them?

A

Headaches, nausea and visual disturbances

You get a mixture of hormone excess and deficiency - hard to diagnose

Large pituitary adenomas (functioning/non-functioning)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What is pituitary apoplexy?

A

Infarction/haemmorhage of the anterior pituitary causing headache, collapse, visual loss (bitemporal quadrantopia) and death.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

How is pituitary apoplexy managed?

A
  1. Resus with fluids and IV steroids
  2. MRI to diagnose
  3. Surgical decompression
  4. Replace deficient hormones
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What are the primary causes of hypoadrenalism?

A

Addisons disease (autoimmune) Glucocorticoid + mineralocorticoid deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What are the secondary causes of hypoadrenalism?

A

ACTH pituitary deficiency Only glucocorticoid deficiency as mineralocorticoids are controlled by RAAS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What are the clinical features of hypoadrenalism?

A

Malaise Weight loss N&V Abdo pain Postural hypotension Hypoglycaemia Adrenal crisis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What electrolyte disturbance do you get in hypoadrenalism?

A

Low sodium, high potassium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

How can you distinguish between a primary and secondary cause of hypoadrenalism?

A

Do synacthen test (synthetic form of ACTH) Measure baseline cortisol, give 250mcgrams synachten IM, measure cortisol at 0,30,60 mins

Healthy - cortisol levels should double

Primary - subnormal response to ACTH as the problem lies within the adrenal gland

Secondary - dramatic increase in cortisol levels as problem lies with pituitary ACTH deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Which individuals would get pigmented skin and salt cravings?

A

Primary adrenal insufficiency Skin - due to increased ACTH Salt cravings - mineralocorticoid deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

How is adrenal insufficiency managed?

A

Primary - hydrocortisone + fludrocortisone Secondary - hydrocortisone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What are the features of a patient with Addisons Disease

A

Lean, TANNED, tired, tearful, dizzy, faints, mood disorders - very non-specific

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What causes an adrenal crisis?

A

Severe stress - accident/infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What are the features of an adrenal crisis?

A

Hypovolaemic shock, abdo pain, vomiting, hypoglycaemia, confusion (severe low na) and fever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

How is an adrenal crisis managed?

A
  1. 1 litre 0.9% saline STAT
  2. 100mg IV hydrocortisone STAT, then 200mg/24hr
  3. Correct hypoglycaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What is the role of aldosterone?

A

Promotes sodium and water retention Lowers plasma potassium levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What are the exogenous causes of Cushing’s syndrome (adrenal excess)?

A

Steroids (RA, asthma)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What are the endogenous causes of Cushing’s syndrome?

A

Adrenal tumour (benign/malignant)

Pituitary tumour that secretes ACTH (Cushings disease)

Ectopic ACTH secreting tumours (SCLC, carcinoid)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What are the symptoms and signs of Cushings syndrome?

A

Moon face, plethora, buffalo hump, thin hair/skin/nails, striae, central wasting, acne, hirsutism, malaise, depression, bruising, DM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

How is Cushings syndrome investigated?

A

24 hour urinary free cortisol excretion AND Overnight dexamethasone suppression test (levels will be >280 and no cortisol suppression respectively) If tumour is suspected, do CT/MRI to investigate.

If ectopic suspected, administer metyrapone - if cortisol is still high, the ACTH is coming from an ectopic source

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

How can you localise the cause of Cushing’s syndrome?

A

Do plasma ACTH levels Low ACTH = adrenal tumour (due to feedback mechanism) –> do CT High ACTH = pituitary or ectopic

High dose dexamethasone test:

<90% drop in urinary cortisol - ectopic ACTH

>90% drop - pituitary adenoma (cushings disease)

Then do corticotrophin releasing test, cortisol will rise with pituitary disease but not ectopic (as it is not connected)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

How is Cushings syndrome managed:

a) Adrenal tumour
b) Cushings disease
c) Ectopic secretion

A

a) removal of adrenals, radiotherapy
b) resection of pituitary adenoma, metyrapone
c) surgery, radiotherapy

For all, treat comorbidites and stop exogenous steroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What is the role of aldosterone?

A

Stimulation of sodium and water absorption Removal of potassium from circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What are the 3 ways in which aldosterone secretion is managed?

A
  1. RAAS - levels rise in response to low BP and renin release
  2. Potassium - directly stimulated aldosterone secretion
  3. ACTH - this is minor!!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What are the symptoms of hyperaldosteronism?

A

Hypertension!! Usually asymptomatic other than this

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What does biochem show for hyperaldosteronism?

A

Decreased K and Mg

Metabolic Alkalosis

Primary - decreased renin

Secondary - increased renin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What are the primary causes of hyperaldosteronism?

A

Conn’s syndrome - adrenal adenoma Bilateral adrenal hyperplasia (MOST COMMON) Adrenal carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What are the secondary causes of hyperaldosteronism?

A

Any condition which increases renin production!! eg. renal artery stenosis, HF, liver failure, nephrotic syndrome Barrters syndrome Gitelmanns syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

How is Conn’s syndrome managed?

A

Laparoscopic adrenelectomy

Spironolactone (aldosterone antagonist) to control BP/K before op

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What are the causes of primary hypothyroidism?

A

Hashimoto’s thyroiditis (autoimmune) Surgery (eg. for hyperthyroid) Radiotherapy Iodine deficiency Drugs (amiodarone, lithium, iodine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

What are the causes of secondary hypothyroidism?

A

Pituitary deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What are the symptoms of hypothyroidism?

A

Weight gain Hair loss (particularly lateral part of eyebrow) Cold intolerance Depression Fatigue Menorrhagia Constipation Dry Ataxia Ascites Bradycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

How is hypothyroidism diagnosed?

A

Primary - increased TSH, low T3/T4 Secondary - normal TSH, low T3/T4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

How is hypothyroidism treated?

A

Levo-thyroxine NB only use TSH to guide treatment in primary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What is Hashimotos Thyroidits?

Describe typical presentation

What anitbodies would be present?

A

A type of primary hypothyroidism, due to autoimmune attack of the thyroid, that is associated with T1DM, Addison’s or Pernicious anaemia. It may cause transient thyrotoxicosis in the acute phase. It often presents as a goitre in women aged 60-70 years old.

Anti-TPO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

What are the causes of secondary hyperthyroidism?

A

Pituitary TSH, usually due to a TSHoma (very rare)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What are the causes of primary hyperthyroidism?

A

Graves disease Toxic nodule/goitre

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What are the symptoms of hyperthyroidism?

A

Weight loss Intolerance to heat Ammenorhea Fatigue Anxiety Palps Diarrhoea Brisk reflexes Pretibial myxoedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Name 3 specific signs to Graves

What autoantibody would be present?

A

Orbitopathy

Thyroid associated dermopathy

Thyroid acropachy (clubbing)

TRab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

How is hyperthyroidism diagnosed?

A

Primary - low TSH, high T3/T4 Secondary - normal TSH, high T3/T4

NB - patients may have a thyroid bruit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

How is a TSHoma managed?

A

Use somatostatin analogues (methimazole) Remove TSHoma with transphenoidal surgery

98
Q

How is hyperthyroidism managed?

A

Inhibit fT4 to fT3 - Carbimazole, propylthioruracil

Symptom control - B blockers (propanolol)

Radioiodine (but will lead to hypothyroidism)

Remember - if pt gets a sore throat on carbimazole go to A&E as it might be agranulocytosis

99
Q

What is a thyroid storm and what are the features?

A

Severe hyperthyroidisim causing tachycardia, fever, encephalopathy, fits, stroke, hypertension, D&V, circulatory collapse and death. It is a medical EMERGENCY.

100
Q

How is a thyroid storm treated?

A

Propylthiouracil

Iodine

Steroids(hydrocortisone)

Beta-blockers (propanolol)

IV fluids

101
Q

What is a myxoedema coma?

A

Severe hypothyroidism causing hypothermia, bradycardia, coma, seizures, cyanosis, decreased BP and heart failure

102
Q

How is a myxoedema coma treated?

A

Tri-iodothyronine Steroids (hydrocortisone) IV fluids Active warming for hypothermia

103
Q

What is subclinical thyroid disease? Why is it clinically significant?

A

When TSH levels are changed but T3/T4 are normal Increased risk of CVS disease and osteoporosis

104
Q

What is sick euthyroidism?

A

This is the derangement of TFTs in any systemic illness - typically everything will be low. DO NOT TREAT

105
Q

What is Graves Eye Disease

A

Eye discomfort, grittiness, photophobia, afferent pupillary defect and expothalmous. This is associated commonly with Graves’ disease but can be present in any thyroid disorder.

106
Q

What would a normal thyroid uptake scan show?

A

Diffuse, even uptake of radioactive iodine

107
Q

What would a graves thyroid uptake scan show?

A

Diffuse, increased uptake of iodine as the entire gland is overactive

108
Q

What would a hashimotos thyroid uptake scan show?

A

Diffuse, decreased uptake of iodine as entire gland is underactive

109
Q

What would a multinodular goitre show on thyroid uptake scan?

A

Focal areas of increased and decreased uptake

110
Q

What is a hot/cold nodule?

A

An area which shows a small bit of increased/decreased uptake of radioactive iodine This requires investigation with USS FNA as it could be malignant (particularly cold) If hot it may require ablation, resection or medication

111
Q

Name 3 causes of diffuse neck lumps

A

Simple goitre

Thyroiditis

Iodine deficiency

112
Q

Name 4 causes of nodular neck lumps

A

Multinodular goitre

Solitary toxic nodule

Cysts

Fibrosis

113
Q

Name 2 causes of miscellaneous goitre/neck lumps

A

Sarcoidosis TB

114
Q

Name 4 causes of neck tumours

A

Benign adenoma Carcinoma (papillary, follicular, medullary, anaplastic) Lymphoma Mets

115
Q

What is De Quervains Thyroiditis (subacute)? Describe the stages of its development.

A

POST INFECTION thyroiditis 1. Initial follicular destruction 2. Release of thyroid hormones causing hyperthyroidism 3. Temporary hypothyroidism 4. Resolution or progression to longterm hypothyroid

Patients will be post infection, and may have a painful neck.

116
Q

What is acute thyroiditis?

A

Thyroiditis following a suppurative infection

117
Q

What is silent thyroiditis?

A

Similar progression to subacute but NO PAIN and common in post-partum period

118
Q

What are some congenital causes of primary hypogonadism?

A

Klinefelters syndrome (47XXY) Cryptorchidism (absence of testes) Turners syndrome (45X) Gonadal dysgenesis

119
Q

Describe a patient with Klinefelters syndrome

A

Tall, gynaecomastia, reduced body hair, low libido, osteoporosis

120
Q

What are some acquired causes of primary hypogonadism?

A

Infection (mumps/HIV) Autoimmune (premature ovarian failure/PCOS) Iatrogenic (chemo) Infiltrative (haemochromatosis) Drugs (ketoconazole)

121
Q

What are some causes of secondary hypogonadism?

A

Pituitary deficiency

122
Q

What are the clinical features of hypogonadism?

A

Libido loss Osteoporosis (low oestrogen) Amennhorea Erectile dysfunction

123
Q

How is hypogonadism treated?

A

Replacement of sex steroids (give testosterone if <8nmol/l, with 12 weekly injections or daily gels) –> keep an eye on the haematocrit Address fertility issues (exogenous gonadotrophin - only works in secondary)

124
Q

How are prolactin levels normally regulated?

A

Dopamine pathway, dopamine suppresses prolactin

125
Q

What are the physiological causes of raised prolactin?

A

Pregnancy Stress

126
Q

What are the pathological causes of raised prolactin?

A
  • Drugs (metoclopramide, TCAs, antipsychotics, methyldopa) - Prolactin secreting pituitary adenomas - Stalk hyperprolactinaemia (non functioning tumour) - Hypothyroidism - Cirrhosis - Renal failure - Sarcoid
127
Q

What are the symptoms of raised prolactin?

A

Men - erectile dysfunction, visual defects, headache, osteopenia Women - galactorrhoea, infertility, menstrual changes

128
Q

How is raised prolactin treated?

A

Dopamine agonists eg. bromocriptine, cabergoline, quinagolide

129
Q

What causes acromegaly?

A

Pituitary MACROadenoma (nearly always)

130
Q

What are the features of acromegaly?

A

Coarse features Sweating Organomegaly Carpal Tunnel Osteoarthritis Visual field defects from macroadenoma OSA HTN CVS disease Slightly increased cancer risk

131
Q

How is acromegaly diagnosed?

A

Failure of oral glucose tolerance test

132
Q

How is acromegaly managed?

A

Transphenoidal surgery Somatostatin/dopamine agonists Pegvisomant (v expensive!!)

133
Q

What is diabetes insipidus?

A

Deficiency in vasopressin causing polyuria, nocturia thirst and dehydration

134
Q

What are the central (secondary) causes of DI?

A

Congenital Idiopathic Head injury Pituitary adenoma Infection and inflammation

135
Q

What are the nephrogenic (primary) causes of DI?

A

Kidney tubules don’t respond to ADH

136
Q

What electrolyte abnormality is seen in DI?

A

Hypernatremia Increased serum osmolality

137
Q

How is DI managed?

A

Desmopressin

138
Q

When should a neck USS be done?

A

Non-functioning nodules

139
Q

What is the 1st line treatment for Cushings disease?

A

Transphenoidal surgery

140
Q

How can Conns syndrome be screened for? What measures should be taken before doing the test?

A

Aldosterone:renin ratio - Higher the ratio, more likely the diagnosis

Make sure potassium is normal

Stop diuretics, b blockers, NSAIDs, ACEis, ARBs

Do CT/MRI to diagnose adenoma

141
Q

What test is used to investigate DI?

A

Water deprivation test - despite this patient will still produce dilute urine

142
Q

What are the indications for total thyroidectomy?

A

Rapid control needed

Severe Graves eye disease

143
Q

What is T3 toxicosis?

A

Autonomous nodule low TSH, normal T4, high T3

144
Q

How is a dexamethasone test carried out?

A

1mg dexamethasone administered at midnight, cortisol checked at 9am If cortisol <50, unlikely to be bushings

145
Q

What is a phaeochromocytoma?

A

Adrenomedullary catecholamine secreting tumour

146
Q

What are the symptoms of phaeochromocytoma?

A

HTN General systemic ‘anxiety’ symptoms Headache Cardiovascular (chest pain, palps)

147
Q

What investigations should be done for pheochromocytoma?

A

Plasma mets (suspcious if 3x the norm)

24hr urine metadrenalines

CT scan

IMIBG scan - exclude multiple tumours

148
Q

What is a potential complication of phaeo?

A
  • Prone to haemmorhage and necrosis - Fatal hypertensive crisis
149
Q

How is phaeo treated: a) conservatively b) medically c) surgically?

A

a) high salt and fluid diet b) a blockers c) laparoscopic removal

150
Q

Which endocrine conditions give you HTN?

A

Adrenal - cushings, phaeo, conns

Parathyroid - hyperparathyroidism

Pituitary - cushings, acromegaly

Thyroid - both can

151
Q

What are the functions of calcium ?

A
  • Transmits nerve impulses
  • Maintains cell wall permeability
  • Activates clotting
  • Heart muscle contraction
  • Bones and teeth
152
Q

What are the functions of phosphorus?

A
  • Bone formation
  • Energy production
  • Carb/protein/fat metabolism
  • Maintains acid base balance
153
Q

What is the function of PTH?

A

Regulates calcium and phosphorus - when serum ca is low, PTH increases calcium resorption from the bone and calcium reabsorbtion from the kidney.

It causes phosphate excretion by blocking its reabsorption in the kidney

154
Q

What are the causes of hyperparathyroidism?

A

Parathyroid hyperplasia/adenoma/carcinoma

155
Q

What are the complications of primary hyperparathyroidism?

A

Kidney stones

Osteoporosis

Osteitis fibrosis cystica

Brown tumours

Corneal calcification

HTN

‘stones, bones, groans and moans’

156
Q

How is primary hyperparathyroidism managed?

A

Surgical neck exploration Conservative Calcimimetic drugs

157
Q

What causes hypercalcemia?

A
  • Malignancy (ectopic, bone erosion)
  • Drugs
  • Hyperparathyroidism
  • Vit D and calcium intake
  • Sarcoidosis
158
Q

How is severe hypercalcemia managed?

A
  1. Do baseline PTH (if low = cancer, if high = primary PTH)
  2. IV saline
  3. IV bisphosphonates
159
Q

What are the symptoms of hypercalcemia?

A

Lethargy, fatigue

Bone/kidney pain (kidney stones)

Depression

Anorexia

Constipation

HTN

160
Q

What would an ECG of someone with severe hypo/hypercalcemia look like?

A

hyper - short QT interval hypo - long QT interval

161
Q

What causes hypocalcemia?

A
  • Hypoparathyroidism - Vit D defieciency - Drugs (bisphos, chemo) - Renal failure - Severe illness
162
Q

What are the symptoms of hypocalcemia?

A

TINGLING, TWITCHING, TETANY, TROUSSEAS CHVOSTEKS AND SEIZURES

163
Q

What are the complications of hypocalcemia?

A
  • Osteoporosis - Arrhythmia
164
Q

How is severe hypocalcemia treated?

A

ACUTE - calcium chloride DONT DO IF CHRONIC

165
Q

What is Trousseas sign?

A

Forearm muscle spasm following cuff inflation, sign of tetany

166
Q

What is Chvosteks sign?

A

Hyper excitability of facial nerve, sign of tetany

167
Q

What investigations should be done for someone with bone disease?

A

Calcium, phosphate, PTH Xray, DEXA?

168
Q

What is osteoporosis? How is it diagnosed?

A

Low bone density (T score -2.5 on BMD)

169
Q

What are the RF for osteoporosis?

A

Smoking

Steroids

Early menopause

Calcium intake

Fam hx

Endocrine problems

Renal disease

170
Q

What is osteomalacia? How is it diagnosed?

A

Softening of bones due to low calcium, phosphate and vit D, elevated PTH, ALP

171
Q

What are the RF for osteomalacia?

A

Low calcium, vit D sunlight Renal hepatic disease Drugs

172
Q

What are the X-ray appearance of osteomalacia?

A

Cupped epiphyses

Loosers zones

Rachitic rosary

173
Q

What are the symptoms of hypomagnesia?

A

Tremors, tachycardia, confusion

174
Q

What are the symptoms of hypermagnesia?

A

Vasodilation, hypotension, vomiting

175
Q

What causes hypomagnesia?

A

Alcoholism Malnutrition

176
Q

What causes hypermagnesia?

A

Renal failure Untreated DKA

177
Q

How is T2DM diagnosed (3 ways)

A

Random blood glucose >11.1 in presence of symptoms OR Random blood glucose >11.1 on two occasions with no symptoms

HbA1c > 6.5% (48mmol/mol) (39-46mmol/mol = pre-diabetes) - this is better for checking degree of diabetes control rather than diagnosis

178
Q

What factors can affect HbA1c, and make it invalid as a diagnostic tool?

A
  • Conditions with increased red cell turnover eg. acute blood loss, pernicious anaemia, haemolytic anaemia, malaria, haemoglobinopathies
  • Pregnancy
  • Liver and renal disease
  • Ethnic variations
179
Q

Describe the pathophysiology behind Type 1 diabetes

A

Insulin deficiency due to autoimmune attack of beta cells in the pancreas Linked to HLA D3/4

180
Q

Describe the pathophysiology behind Type 2 diabetes

A

Acquired insulin resistance due to the body being unable to meet the requirement for insulin.

181
Q

What conditions can cause secondary diabetes?

A
  • Acromegaly
  • Cushing’s syndrome
  • Haemochromatosis
  • Pancreatitis
182
Q

Describe the pathophysiology behind gestational diabetes

A

Excessive production of counter-insulin hormones (cortisol,oestrogen), produced during pregnancy, leading to a state of insulin resistance in the mother

183
Q

Which patients are prone to ketoacidosis?

184
Q

Which patients usually are diagnosed through the complications that have arisen as a result of their diabetes?

185
Q

Who gets screened for T2 diabetes?

A
  • Women with previous gestational diabetes - People aged 65 and over - Afro caribbean and south asians aged 35 and over - People over 50 who have BMI>30, T2DM first degree relative or hypertension - People with clinical cardiovascular disease - Women who are obese and have polycystic ovary syndrome
186
Q

What measures can reduce microvascular complications of diabetes?

A

Tight blood glucose control (FBG<5.5)

187
Q

What measures can reduce macrovascular complications of diabetes?

A

Tight blood pressure control (<130/80)

188
Q

What measures can decrease the incidence of cardiovascular events in diabetes?

A

Control of lipids (T.chol<4)

189
Q

What are the microvascular changes seen in diabetes?

A

Retinopathy, nephropathy, neuropathy, erectile dysfunction, absent foot pulses, ischaemic skin chances

190
Q

What are the macrovascular changes seen in diabetes?

A

Ischaemic heart disease, cerebrovascular disease, peripheral vascular disease

191
Q

How can diabetic foot be managed?

A
  1. Examine feet of all those with diabetes 2. Suspect: infection, fracture, ulceration, Charcot 3. Investigations: WBC, CRP, ESR, U&E, Swab, X-ray 4. Treatment: bed rest, IV abx, refer
192
Q

What does infection cause DKA?

A
  1. Infection leads to high cortisol and catecholamines 2. These cause gluconeogenesis
193
Q

How is DKA diagnosed?

A

Glucose > 11 mmol/l Ketones > 3 mmol/l Acidosis <7.3 pH

194
Q

What is the pathophysiology behind DKA?

A
  1. Glucose cannot be broken down as there is no insulin 2. The body breaks down fatty acids to get ketones for energy 3. This causes acidosis
195
Q

What are the signs and symptoms of DKA?

A

SYMPTOMS: Polyuria, polydipsia, weight loss, weakness, drowsiness, coma SIGNS: dehydration, hypovolaemia, increased respiration

196
Q

What is the protocol for DKA?

A

ABCDE

  1. IV fluids
  2. IV fluids + potassium
  3. IV insulin infusion
  4. Investigations to see what causes DKA, treat cause
  5. Establish monitoring regimen
  6. Once insulin in normal range, switch to glucose-insulin infusion to prevent hypos
197
Q

What are the pros and cons of the oral glucose tolerance test?

A

Pros - sensitive, early marker of impairment Cons - affected by short term lifestyle changes, expensive, takes time and effort

198
Q

What are the pros and cons of the glycated haemoglobin concentration (HbA1c)

A

Pros - reflects long term glucose, unaffected by acute change, convenient, high correlation with risks of complication Cons - lower sensitivity, expensive, not recommended for rapidly progressing diabetes

199
Q

What is metabolic syndrome?

A

Central obesity + 2 of: - High triglycerides - High BP - Low HDL - High fasting glucose - DM This can cause vascular events

200
Q

How can glucose control be monitored?

A

HbA1c, finger prick test (if on insulin)

201
Q

What is the definition of hypoglycaemia?

A

Plasma glucose <3

202
Q

What are the symptoms of hypoglycaemia?

A

AUTONOMIC - sweating, anxiety, hunger, tremor, palpitations NEUROGLYCOPENIC - confusion, drowsy, seizures, coma

203
Q

What causes hypoglycaemia EXPLAIN?

A

EXogenous drugs (insulin) Pituitary insufficiency Liver failure Addison’s disease Islet cell tumours Non-pancreatic neoplasms

204
Q

How is a hypoglycaemic attack managed?

A

ABCDEFG (dont ever forget glucose)

Conscious - oral glucose

Unconscious

  • IV dextrose, glucogel, IM glucagon
  • monitor BMs every 15 min
  • give long acting carbohydrate
  • review medication
205
Q

What is impaired awareness of hypoglycaemia?

A

Normally the autonomic symptoms of a hypo will kick in before the neuroglycopenic ones.

In long term diabetics, this will not happen so you wont get the usual warning signs

206
Q

What are the features of background diabetic retinopathy?

A

Dots, blots and deposits

207
Q

What are the features of pre-proliferative diabetic retinopathy?

A

Cotton-wool spots, haemorrhages and venous beading

208
Q

What are the features of proliferative diabetic retinopathy?

A

New vessel formation

209
Q

How can diabetes affect the eyes?

A

Retinopathy, maculopathy, blurred vision, cataracts, rubeosis iridis

210
Q

What is rubeosis iris?

A

New vessel formation on the eye, leading to glaucoma

211
Q

What are the signs of neuropathy in the feet?

A

Decreased sensation, absent ankle jerks, deformity

212
Q

What is Charcot’s foot?

A

A condition in which sugar damages the bones of the foot, causing weakness

213
Q

What is a hyperosmolar hyperglycaemic state?

A

T2DM - extremely high blood glucose causing severe dehydration, dry skin, confusion, coma

214
Q

How is hyperosmolar hyperglycaemic state diagnosed?

A

Glucose >30mmol/l and ABSENCE OF DKA FEATURES (vomiting)

215
Q

How is HH state managed?

A

IV fluids slowly and electrolyte replacement (potassium)

216
Q

What is the relevance of a C-peptide level under 0.51mg/ml?

A

It could indiate T1DM - C-peptide is a surrogate marker for endogenous insulin as C-peptide and insulin both originate from pro-insulin

217
Q

Which antibodies can be used in T1DM diagnosis, when clinical diagnosis is uncertain?

A

GAD

IA-2

ICA

218
Q

What are the diagnostic criteria for gestational diabetes?

A
  • Fasting plasma > 5.6mmol/L
  • 2hr plasma glucose >7.8mmol/L
219
Q

How are diabetics managed during:

a) pregnancy?
b) labour?

A

a) folic acid 5mg, monitor BM/ketones
b) GKI infusion to maintain blood glucose 4-7 during labour. Monitor BM every 30-60 mins during this period. Reduce insulin rate post partum.

220
Q

What are the indications for GD screening?

A
  • BMI>30
  • Previous macrosomic baby >4.5kg
  • Previous GD
  • Family history
  • High risk ethnic minority
221
Q

What is MODY? What are the two main types?

A

Maturity Onset Diabetes of the Young

This is diabetes caused by a inherited mutation in a gene involved in insulin production. The two main types are:

  • Glucokinase
  • Transcription factor
222
Q

What are the key diagnostic features in MODY?

A
  • Diagnosis under the age of 25
  • Two or more generation family hx of diabetes
  • Residual insulin secretion over 3yrs after supposed T1DM diagnosis
  • Lack of metabolic syndrome in supposed T2DM diagnosis
223
Q

What is the pathology of glucokinase MODY?

A

Mutation in glucokinase leading to a higher threshold for glucose stimulated insulin secretion, so blood glucose levels are slightly higher than normal

224
Q

How does glucokinase MODY present and how should it be treated?

A

It is asymptomatic so usually only picked up through routine testing (eg. in pregnancy)

Only treat in pregnancy

225
Q

What is the pathology of transcription factor MODY?

A

Mutation in one of the transcription factors involved in pancreatic development, causing impaired insulin secretion>

Factors affected:

HNF1a

HNF1b

HNF4a

226
Q

How does transcription factor MODY present and how is it treated?

A

HNF1a/4a - normoglycemic in childhood, develop symptoms of diabetes at 12-30yrs

Treat with low dose sulphonylureas

HNF1b - may present with pancreatic atrophy/renal cysts/genitourinary abnormalities

Treat with insulin

227
Q

What is a lipodystrophy syndrome? What are the two main types and their features?

A

Complete or partial absence of adipose tissue, with associated insulin resistance. Diagnose clinically.

Congenital generalised - develop DM in 10-20yrs, big appetite, autosomal recessive

Familial partial - loss of fat in lower body and arms, excess fat in face and trunk

228
Q

A patient presents with a chubby face and trunk and very thin legs and arms. What is the diagnosis?

A

Familial partial lipodystrophy syndrome

229
Q

Describe 3 clinical features of insulin resistance

A
  • Persistent hyperglycaemia despite large doses of insulin
  • Acanthosis nigricans
  • PCOS
230
Q

Name 5 heritable conditions that have associations with diabetes mellitus

A

Turners

Klinefelters

Downs

Prader Willi

PCOS

Lawrence-moon

231
Q

Describe the features of temporary and permanent neonatal diabetes

A

Presents before 6 months with high glucose levels or DKA, low birth weight and low C-peptide

This may progress to permanent, in which you would start to see added neurological features

232
Q

What is the pathophysiology of neonatal diabetes?

A

GOF mutation in beta cell K ATP channel - K channel cannot respond to ATP so is permanently open. This means there is no beta cell depolarisation and no insulin release.

Eg. KCNJII/ABCC8 genes

233
Q

Why do HIV treated patients have a 4 fold risk of DM?

A

Protease inhibitors (component of HAART) cause increased insulin resistance

Indanavir increases hepatic glucose production

234
Q

What is central salt wasting syndrome?

A

A rare endocrine condition featuring low serum Na and dehydration in response to brain injury

235
Q

What is latent autoimmune diabetes?

A

Presents with features of T1DM in adulthood

Symptoms persist despite diet and medication

Presence of islet cell antibodies

236
Q

What is a side effect of insulin injection?

A

Lipohypetrophy

237
Q

What is Kallman syndrome?

A

Hypogonadism + infertility + hypo-anosmia

238
Q

How do you calculate the anion gap?

A

(sum of all positive ions) - (sum of all negative ions)

Normal = 8-10 (diarrhoea, renal tubular acidosis, hyperparathyroidism)

High = lactic acidosis, ketoacidosis, salicylate overdose

239
Q

What is the best way of investigatin a pituitary tumour?

4TH YEAR - CSIM2 (20 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions