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Endocrine Flashcards

1
Q

Jacky, 30, has had a range of persisting symptoms, which doctors believe is down to hypoadrenalism. Which symptom would distinguish between primary adrenal failure and secondary adrenal insufficiency?

A

Skin hyperpigmentation

Seen in primary adrenal insufficiency (as this will have high ACTH)

Not seen in secondary as this has low ACTH

Hyperpigmentation is caused by melanin stimulating hormone (which has same pre-cursor as ACTH)

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2
Q

Name 4 common features of multiple myeloma

A 
CRAB
C- hyperCalcaemia 
R- Renal failure 
A - Anaemia (and thrombocytopenia)
B - Bone fractures or lytic lesions or bone pain

Investigate: Serum elecrophoresis looking for a monoclonal band

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3
Q

What presenting symptoms and investigation results characterise diabetes insipidus?

A

Polyuria and polydipsia
High serum osmolality and low urine osmolality

(High urine osmolality would rule out DI)

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4
Q

What steroids are highly mineralocorticoid and which highly glucocorticoid? What side effects do each have?

A

Mineralocorticoid = Fluid retention, HTN
- Fludrocortisone

Glucocorticoid = Immune suppresion plus all normal steroid SE (endocrine, GI, pysch, cushings etc)
- Dexamethosone

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5
Q

What is indicated by raised ferritin levels?

A

Either iron overload (10%)
OR
Inflammation (90%) - note ferritin is an acute phase protein

Transferin saturation <50% excludes iron overload

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6
Q

A 41-year-old woman presents with palpitations and heat intolerance. On examination her pulse is 90/min and a small, diffuse goitre is noted which is tender to touch. Thyroid function tests show the following:

Free T4 24 pmol/l
TSH < 0.05 mu/l

What is the most likely diagnosis?

A

Thyrotoxicosis with tender goitre = subacute (De Quervain’s) thyroiditis

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7
Q

Name 3 ECG changes associated with hyperkalaemia?

A

Prolonged PR
Wide QRS
Peaked/ tented T waves

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8
Q

What are the three categories and six most common causes of hyponatremia?

A

Na < 135

Hypovolemic: Diuretics or Addisons
Euvolemic: SIADH
Hypervolemic: Heart/ liver/ renal failure

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9
Q

How do you treat hyponatremia in acute and chronic situations?

A 
PLUS TREAT UNDERLYING CAUSE
Acute (<48hrs) = 3% hypertonic saline 
Chronic:
- Hypovolemic = 0.9% isotonic saline 
- Euvolemic = Fluid restriction
- Hypervolemic = Fluid restriction (plus furosemide if underlying condition warrants it)
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10
Q

What are the symptoms of hyponatremia? (5)

A 
Confusion, headache, balance difficulty
Altered mental status
Seizures/ coma 
Orthostatic hypotension 
Low urine output, decreased JVP, dry mucus membranes, poor skin turgor
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11
Q

What are the most common causes of hypernatremia? (5)

A

Water loss
- Hyperglycemia
- Loop diuretics
- Diabetes insipidus (not enough ADH to reabsorb water)
- Severe diarrhoea, sweating, burns, vomitting etc
Not enough water gain
- Limited intake of water
Sodium gain
- Cushings (= increased glucose, sodium retention with the water retention)
- Primary aldosteronism (resets regulation of ADH secretion)

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12
Q

How do you manage hypernatremia?

A

Oral or IV fluids

Plus treat underlying cause

  • If water loss may need desmopression (Diabetes insipidus)
  • If excess sodium and fluid overload may need loop diuretic
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13
Q

What are the definitions of hyperkalaemia?

A

Mild - 5.5-5.9 mmol/L.
Moderate - 6.0-6.4 mmol/L.
Severe - >6.5 mmol/L.

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14
Q

What are the main causes of hyperkalaemia? (4 groups)

A

DRISP
Drugs (ACEI, ARBs, NSAIDS, heparin)
Renal (AKI/ CKD/ addisons)
Increase in production (Tumour lysis syndrome, trauma, burns)
Shift from intracellular to extracellular (DKA)
Pseudo (long tourniquet time, clenched fist, test tube haemolysis)

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15
Q

Name 3 symptoms of hyperkalaemia?

A

Usually non specific weakness and fatigue

Can get muscle paralysis, SOB and bradycardia

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16
Q

What investigations should be done on a patient with hyperkalaemia? (4)

A 
Repeat K+
ECG
Glucose 
FBC
ABG
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17
Q

Name 3 changes on an ECG associated with hyperkalaemia?

A 
Peaked T waves
Prolonger PR (>200)
Wide QRS (>120)

Hyperkalaemia can cause conduction disturbances!

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18
Q

How should hyperkalaemia be managed is K+ is 7.1?

A

SEVERE: Urgent ABCDE
- ABG to give immediate determination if true result, perform ECG

1) 10ml 10% Calcium gluconate to protect heart (works in 1-3mins, lasts 30-60mins). Keep giving upto 50ml until ECG improvement

2a) Insulin-glucose infusion (10units with 25g glucose) - moves K+ into cells. NB: K+ should come down 0.5-1 over 15mins
2b) Nebulised salbutamol (10-20mg should reduce K+ 0.5-1mmol/L in 15-30mins)

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19
Q

How should a K+ of 5.9 be treated?

A

Use calcium resonium (gets K+ out of GI tract, brings down by approx 1mmol but takes 2 hours so no use in acute setting)

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20
Q

How is hypokalaemia classified?

A

Mild - 3.1-3.5 mmol/L
Moderate - 2.5-3.0 mmol/L
Severe - <2.5 mmol/L

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21
Q

What are the three most common causes of hypokalaemia?

A 
Increased water loss:
- Diuretics
- Vomiting/ diarrhoea 
Cellular shift:
- Alkalosis
- Insulin/ glucose
Decreased K+ intake:
- NBM
- Anorexia
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22
Q

How does hypokalaemia present?

A

Generally asymptomatic

Can give weakness, muscle pain, constipation or paralysis

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23
Q

What are the findings in an ECG for a patient with a K+ of 2.9?

A

ECG changes in hypokalaemia:

  • Flat T waves
  • ST depression
  • Prominant U waves
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24
Q

How is hypokalaemia managed? (2)

A

If mild: Dietary suppliments (40-120mmol/day)

If secondary care and severe:
- IV KCL (never bolus, give with normal saline). Needs careful monitoring

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25
Q

You are called to the ward to see a patient with high sugars, roughly how much does 1 unit of insulin cause a BM to drop?

A

1 unit drops blood glucose by approx 3mmol

Remember aiming around 8-10

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26
Q

Name 3 rapid acting insulins? When are they used?

A

Humalog
Novorapid
Apidra
Fiasp

All act rapidly (within 20mins) and have short action (<6hours)

Good for meal time insulin and correcting insulin

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27
Q

When should biphasic insulins be given?

A

At meal times

As contain rapid and intermediate acting insulins

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28
Q

What is the definition of hypoglycaemia?

A

Under 3mmol however in practice any under 4 should be treated

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29
Q

What is a phaeochromocytoma and how does it present?

A

Neuroendocrine tumor of the medulla of the adrenal glands

Present: Raised BP, palpitations, sweating, anxiety

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30
Q

What investigation is done for phaeocrhomocytoma?

A

24 hr urinary metanephrines

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31
Q

What is the treatment pathway for phaeochromocytoma?

A

A- Alpha blocker
B- Beta blocker
C- Cut it out (surgery)

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32
Q

How does congenital adrenal hyperplasia present and what is the most common cause?

A

Kid with precocious puberty and possible sex changes

Due to 21-hydroxylase deficiency

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33
Q

What investigation should be done for congenital adrenal hyperplasia?

A

17-hydroxyprogesterone

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34
Q

What is the function of vasopressin?

A

Vasopressin = ADH

Causes retention of water (solute free)

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35
Q

What is diabetes insipidus and how can causes be categorised?

A

Diabetes insipidus = not enough ADH (so no stopping of diuresis = lots of diuresis)

Therefore presents with polyuria and polydipsia

Cranial cause - Not producing ADH in post pituitary
Renal cause - Not responding to ADH

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36
Q

What is seen on plasma and urine osmolarity in diabetes insipidus?

A

Plasma osmolality = High

Urine osmolality = Low (as lots of fluid in urine so it’s dilute)

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37
Q

What is the first/ second line investigation of diabetes insipidus?

A

1) Water deprivation test
Would expect urine osmolality to rise, if it DOESN’T then this is DI (if it does probably pyschogenic cause of polydipsia)

2) Desmopressin test
- Giving ADH should put things back to normal (raised urine osmolarity). If it does then this is pituitary cause of the DI, if it doesn’t the kidneys aren’t responding to any ADH so renal cause

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38
Q

How do you manage diabetes insipidus?

A

Cranial cause = Give desmopression (ADH)

Renal cause = Supportive, protect kidneys, desmopression may help a bit

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39
Q

What is the action of aldosterone?

A

Promotes water reabsorbtion (via Na+ absorbtion and K+ excretion)
- So spironolactone which inhibits aldosterone causes less reabsorbtion (lowerBP) and less K+ excretion (which is why can cause hyperkalaemia)

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40
Q

What are the features of acromegaly (increased growth hormone 2ndry to pituitary adenoma)

A

Spade hands, increase show size
Large tongue
Excessive sweating and oily skin

Pituitary tumour > Headaches, bitemporal hamianopia

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41
Q

How do you investigate a patient for suspected acromegaly?

A

GH varies throughout day so not diagnostic

Do OGTT with serial GH measurements

  • Normal = GH supressed <2 with hyperglycaemia
  • Acromegaly = No supression of GH
42
Q

How is acromegaly managed?

A

Trans-sphenoidal surgery

Can use somatostatin (GH inhibiting hormone) analogues (octreotide) as an adjunct before surgery

43
Q

What are the diagnostic criteria for T2DM?

A

HbA1c > 48mmol/l
Fasting glucose > 7mmol/L
OGTT > 11.1mmol/L

1 result if symptomatic, 2 if asymptomatic

44
Q

What are the result options for a fasting glucose?

A 
<6.1 = Normal
6.1-7 = Impaired fasting glucose
>7 = Diabetes
45
Q

What are the result options for an OGTT?

A 
<7.8 = Normal
7.8-11.1 = Impaired glucose tolerance
>11.1 = Diabetes
46
Q

What are the driving rules with diabetes?

A

Ok to drive but if more than 1 episode of hypo which required assistance need to contact DVLA

47
Q

What are the characteristics of a DKA presentation?

A

Abdopain, polyuria, polydipsia, pear drop breath, kussmaul breathing, N+V, reduced GCS

Acidosis <7.3
Ketones in urine
Glucose >11mmol
(Diagnositic criteria)

48
Q

How should DKA be treated?

A

ABCDE
Fluids (1L in 1hr, 1L in 2hrs, in 4hrs, in 8hrs)
Insulin (0.1/units/kg/hr)
- Once glucose under 15mmol/l start 5% dextrose also

Investigations for cause: FBC, blood cultures, CXR
CT head if reduced GCS

Note needs continually reassessing

49
Q

What is the presentation of HHS?

A

General weakness, leg cramps, confusion, hypovolemia

Criteria:
Glucose >30mmol/l
Hyperosmotic >320mOs/l
Hypovolemia

Often no acidosis!

50
Q

How is HHS treated?

A

Slow fluid rehydration

  • Watch for reducing osmolarity
  • Only use insulin if acidosis
51
Q

Name 5 presenting symptoms of diabetes?

A 
Polyuria
Polydipsia
Lethargy
Pruritus 
Frequent infections
52
Q

What are your first four steps in T2DM management?

A

1) Lifestyle
2) If HbA1c still over 48mmol/l = Start metformin
3) If HbA1c still over 58mmol/l = Start 2nd
- Sulfonylurea (Gliclazide, glipizide, glimepiride)
- DPP-4/Gliptins (Sitagliptin)
- Thiozolidianoes (Pioglitazone)
- SGLT-2 inhibitor (Dapagliflozin)
4) Add third drug from above

53
Q

What is 5th line management in T2DM?

A

If HbA1c still >58mmol/L on 3 drugs
- If BMI <35 = Start exanitide (GLP-1 analouges)
OR
- Start insulin

54
Q

What are pre and post prandial targets for T1DM?

A 
Pre-prandial = 4-7mmol/l
Post-prandial = <9mmol/l
55
Q

What are the characteristics of MODY?

A 
Young age T2DM
Autosomal dominant (HNF-1alpha)
56
Q

What is the best 1st line tx for MODY?

A

Sulfonylureas
(Gliclazide)

NOT metformin

57
Q

What is the action of glucagon?

A

Increases glucose to increase blood sugar

58
Q

What are the characteristics of SIADH?

A 
No peeing (So high urine osmolarity)
Diluted plasma (So low serum osmolarity)
Often have hyponatermia
59
Q

How is SIADH treated?

A

Depending on cause (Hypo/eu/hypervolemic)

60
Q

What is addisons disease?

A

Primary adrenal insufficiency (low cortisol and low aldosterone)

61
Q

What are the features of addisons disease?

A

Lethargy, weakness, N+V, weight loss, salt craving

Hyperpigmentation (raised ACTH)

Hypotension, hyperkalaemia, acidosis, hyponatremia (all due to low aldosterone)
Hypoglycemia (due to low cortisol)

62
Q

How do you investigate possible adissons disease?

A

Short syncanthen test (give ACTH)

  • Normal = Cortisol will rise >550 within 30mins
  • Addisons = Adrenals not working so no rise in cortisol
63
Q

How is addisons disease treated?

A 
Replace glucocorticoid (hydrocortisone)
Replace mineralocorticoid (fludrocortisone)
64
Q

Other than addisons name three other causes of hypoadrenalism?

A

Primary (Mets, TB, HIV)
Secondary (Pituitary tumour, radiation)

EXOGENOUS GLUCOCORTICOID THERAPY

65
Q

What is Conn’s syndrome?

A

Primary hyperaldosteronism CAUSED by an adrenal adenoma

i.e. all Conn’s is PH but not all PH is Conn’s

66
Q

What are the three key features of primary hyperaldosteronism?

A

Hypertension
Hypokalaemia
Alkalosis

67
Q

What is the first line investigation for primary hyperaldosteronism?

A

Aldosterone/ renin ratio

will be raised in primary hyperaldosteronism

68
Q

How do you manage primary hyperaldosteronism?

A

If Conn’s = Surgery (take out adenoma)

If due to bilateral adrenocortical hyperplasia (70%) = Spironolactone

69
Q

What are the components of the HPA axis?

A

Hypothalmus >(CRH)> Pituitary >(ACTH) > Adrenals > (Cortisol)

70
Q

What are the 4 most common causes of cushings syndrome?

A

Exogenous = Iatrogenic (steroid therapy)

Endogenous:
Cushing disease (80%) - Pituitary tumour releasing ACTH
Adrenal adenoma (10%) 
Ectopic ACTH (5%) i.e. from SCLC
71
Q

Name 5 features of cushing syndrome?

A 
Weight gain
Moon face
Truncal obesity
Easy brusiing
Hirsuitism 
Proximal muscle weakness
Facial plethora
72
Q

What 2 investigations can be performed to diagnose cushing syndrome?

A

Urinary 24hr free cortisol (>280nmol/24hrs = CS)

Low dose (1mg) dext supression test
Normal = Cortisol reduces
CS = No reduction
73
Q

How do you distinguish between pituitary or adrenal causes of cushing disease?

A

High dose (8mg) dex supression test

Pituitary cause = Decrease in ACTH and decrease in cortisol
Adrenal cause =
Decrease in ACTH but NO decrease in cortisol

74
Q

What are the most common causes of an addisonian crisis? (3)

A

Sepsis
Surgery
Steroid withdrawal

75
Q

How should an addisonian crisis be managed?

A

1) 1L saline over 1hr
(with dextrose if hypoglycemic)
2) IV hydrocortisone

76
Q

What are the components of a diabetic foot exam?

A 
Look (Skin, ulcers, swelling)
Feel (Temp, cap refil, pulses)
Move (+gait)
\+
Sensation
77
Q

Name 3 features of a hyperthyroid crisis (thyroid storm)?

A

Hyperpyrexia (>41)
Tachycardia (>140)
N+V, jaundice, diarrhoea, abdo pain, confusion, agitation

78
Q

How should you treat a hyperthyroid crisis (thyroid storm)?

A

1) ABCDE (oxygen, fluids etc)
2) IV propanolol 5mg
3) Carbimazole or propylthiouracil PO
4) Hydrocortisone

If agitation - chlorpromazine

79
Q

What is myxoedema coma?

A

Extreme manifestation of (usually untreated) hypothyroidism

> Hypothyroid features
\+
Apathy, low mood, confusion, cognitive decline and possible coma
Hypothermia (<35.5)
Hypotension, bradycardia
80
Q

How should myxoedema coma be managed?

A

ABCDE

  • Early HDU/ ICU admission
  • Immediate T4 and T3 given IV
  • IV hydrocortisone
  • Broad spectrum AB’s

Correct electrolyte and fluid abnormalities

81
Q

Name 7 common hyperthyroid symptoms?

A 
Weight loss
Heat intolerance
Tachycardia
Diarrhoea
Oligomenorrhoea 
Sweats
Tremor 
Irritability and agitation
82
Q

Name 7 common symptoms of hypothyroid?

A 
Weight gain
Cold intolerance
Bradycardia
Constipation
Menorrhagia
Myalgia/ cramps
Weakness
Thin hair
Dry skin 
Low mood
83
Q

What are the 4 most common causes of hyperthyroidism?

A

Graves (70%)
Toxic multinodular goitre
Subacute (DeQuevains) thyroiditis - post viral
Toxic adenoma

84
Q

What are three common features of graves disease?

A

Age 40-60
Exopthalmos, opthalmoplegia, lid lag, pretibial myxoedema

(TSH receptor antibodies in 90%)

85
Q

How do you manage hyperthyroidism?

A

Propanolol for rapid symptom relief

Then either:
A - Slowly titrate carbimazole (or propriothiouracil if preg) according to TFT’s
B- High dose carbimazole to block and levothyroxine to replace

Tx for 12-18months then slowly withdrawl

2nd line - Radioiodine
3rd line - Thyroidectomy

86
Q

What are the 6 most common causes of hypothyroidism?

A

Primary atrophic thyroid
Hashimoto’s (Goitre + TPO antibodies)
Iodine deficiency (Worldwide most common)
Drugs/ surgery (amiodarone/ lithium)
Sick euthyroid (precipitated by illness) - Low TSH
Pituitary tumour - Low TSH

87
Q

What is sub-clinical thyroid disease and how is it managed?

A

Low or high TSH with a normal T3/T4

  • Treat if symptomatic, otherwise observe 6 monthly
88
Q

How do you treat hypothyroidism?

A

Levothyroxine (0-100mcg)

- Half life is 7 days so wait 4 weeks between changing doses

89
Q

What is the most useful marker to monitor progression of a thyroid carcinoma?

A

Serum thyroglobulin

90
Q

What are the most common types of thyroid cancer?

A 
Papillary carcinoma (70%) - Young females, excellent prognosis
Follicular adenoma (20%)
91
Q

How should papillary carcinomas or follicular adenomas of the thyroid be managed?

A

Total thyroidectomy
Followed by radioiodine

Yearly thyroglobulin levels to detect early recurrent disease

92
Q

What is the typical bone profile and clinical features of primary hyperparathyroidism?

A

Bone profile:
- Raised PTH, raised Ca, low Phosphate
Clinical:
Asymptomatic or recurrent abdo pain (pancreatitis/ renal colic)

93
Q

What is the most common cause of primary hyperparathyroidism?

A

Adenoma (80%)

94
Q

What is the typical bone profile and clinical features of secondary hyperparathyroidism?

A

Bone profile:
- Raised PTH, low Ca, high phosphate, low VitD
Clinical features:
- Bone disease
(Secondary hyperparathyroid often due to CKD)

95
Q

What is the most common cause of secondary hyperparathyroidism?

A

CKD

96
Q

How is primary hyperparathyroidism managed?

A

Surgery

97
Q

How is secondary hyperparathyroidism managed?

A

Medical

Calcium and vitD supplimentation

98
Q

How do you differentiate between primary atrophic hypothyroid and hashimoto’s?

A

Primary - No goitre

Hashimoto’s- Goitre, likely TPO antibodies

99
Q

What is the second line diabetic management drug (after metformin) most commonly for a) Obese patients and b) non-obese patients?

A

a) Sitagliptin (DPP-4 inhibitor) - weight neutral
b) Gliclazide (sulfonylurea) - normally best but can cause weight gain (so not in obese) also causes hypo’s so not those at high risk

100
Q

Which acid causes acidosis in DKA?

A

β-hydroxybutyric acid

101
Q

In the cori cycle, where is glucose converted to lactate and vice versa?

A

Glucose > lactate = In liver

Lactate > Glucose = In skeletal muscle

MCHB full (21 decks)

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