Brainscape's Knowledge GenomeTM

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


See full index

Finals > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What is the diagnostic criteria for diabetes

A

symptoms + 1 abnormal blood sugar
asymptomatic + 2 abnormal blood sugars
Abnormal = random >11.1 or fasting >7

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

What HbA1C level would indicate diabetes?

What level would indicate the need to add a drug for a pre-existing diabetic?

A

(48) 6.5% = diagnostic

(58) 7.5% = add agent

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

What are the cons/when would you be cautious about prescribing Metformin?

A

risk of lactic acidosis particularly in renal failure

GI upset

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

What are the cons/when would you be cautious about prescribing Sulphonylureas?
Give an example of one?
When would you consider prescribing them first line over Metformin?

A

Gliclazide

Weight gain
Risk of hypo’s (avoid in lorry drivers)
Hyponatraemia

They are first line in CKD

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

What are the cons/when would you be cautious about prescribing Sitagliptin?
What is a benefit of Sitagliptan?

A

Causes peripheral oedema

Doesn’t cause weight gain
No evidence of hypoglycaemia

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

What are the cons/when would you be cautious about prescribing Pioglitazone?

A

Do not give in HF

ADRs: weight gain, fluid retention, impotence, anaemia, hepatotoxic

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

What are the cons/when would you be cautious about prescribing SGLUT 2 inhibitors?
Give an example of one

A

Dapagliflozon
normoglycaemic ketoacidosis
They cause dehydration, UTIs and fournier’s gangrene

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

Describe rapid acting insulins and give an example

A

Novorapid

Onset within 15 minutes

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

Describe short acting insulins and give an example

A

Actrapid and Humulin S

Onset within an hour

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

Describe intermediate acting insulins and give an example

A

Humulin-I and Insulatard

Onset within 2-4 hours and lasts 20

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

Describe long acting insulins and give an example

A

Glargine and Lantus

Lasts 24 hours

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

What could result in a misleading HbA1C result?

A 
Rapid cell turnover:
haemoglobinopathies
haemolytic anaemia
iron deficiency
CKD
HIV
Medications that increase glucose eg steroids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Why do you get microvascular complications in diabetes? (briefly state pathophysiology)

A

Certain systems do not require insulin to allow glucose uptake. You therefore get osmotic damage to the cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe the stages of diabetic retinopathy

A

pre-proliferative:
mild - microaneurysm
moderate - + blot haemorrhage, hard exudates, cotton wool spots, venous beading
severe - microaneurysm/blot haem in 4 quadrants or venous beading in 2 quadrants

proliferative: neovascularisation leading to vitreous haemorrhage

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

What urine results would you see in diabetic nephropathy?

A

Raised urine albumin/creatinine ratio

>2.5 = microalbuminaemia

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

What do the kidney of a diabetic look like?

A

bilaterally enlarged

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

How do you manage diabetic nephropathy

A

ACE-I or ARB

+ BP control, statins, diet

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

Describe the signs and symptoms of diabetic neuropathy

A

Glove and stocking loss of sensation
Absent ankle reflexes
Charcot foot deformity

Autonomic:
postural hypotension
urinary retention
gastroparesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Describe a diabetic foot ulcer

A

punched out
painless
on a hard callus

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

Describe the signs and symptoms of hyperglycaemia

A 
thirst, dry mouth and frequent urination
abdominal pain
headache
weakness
blurred vision
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How do you treat hypoglycaemia

A

200ml pure fruit juice
1mg IM glucagon
100ml 20% glucose IV

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

What are the hallmark lab results of DKA?

A

acidotic <7.3 with raised anion gap
raised ketones >3
raised blood sugars >11
low bicarbonate <15

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

What is Kussmaul breathing?

A

deep hyperventilation seen in DKA to blow off CO2

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

How do you manage DKA?

A

0.1 units/kg/hour fixed rate
fluids (1L in an hour)
10% dextrose once levels are <14
40mmol K in the fluids if K<5.5

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

What can trigger DKA?

A

infections
surgery
MI
iatrogenic i.e. wrong insulin dose

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

What are the complications of DKA?

A

cerebral oedema
hypokalaemia (due to management of DKA)
VTE
arrhythmias due to electrolyte disturbances

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

How do you manage hyperosmolar hyperglycaemic state?

A

fluids

Only start insulin if there is significant ketones (unlikely as T2 DM and not due to low insulin)

Ensure serum osmolality is regularly monitored - rapid changes can lead to pontine demyelinolysis

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

What do blood sugars have to be for a diabetic to be allowed to drive? And when do they have to check them?

A

> 5

Check them every 2 hours throughout the journey

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

What blood sugars and HbA1C are diagnostic for pre-diabetes

A

fasting 6.1 to 7.0

HbA1C 42-47

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What dietary advice should you give to a diabetic?

A

High fibre
Low fat dairy
Oily fish
Avoid saturated fats and sucrose

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

How would diabetic gastroparesis present and how is it managed?

A

Erratic blood sugar control, bloating, vomiting

Give metoclopramide or domperidone to increase gastric motility

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

Other than ulcers, what else comprises diabetic “foot disease”

A

ischaemia: absent foot pulses, intermittent claudication, gangrene
osteomyelitis
cellulitis
Chacots foot deformity

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

How is hypertension in a diabetic managed?

What is their target BP?

A

ACE-I (no matter what age or ethnicity)

Target is 140/90: the same as non-diabetics

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

What should a diabetic do on a “sick day”?
A) on insulin
B) on metformin
C) on any other oral agent

A

A) ensure to take it
B) take it unless dehydrated as risk of lactic acidosis and renal failure
C) take it

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

How often should a T1DM measure glucose and what should it be?

A

At least 4x/day
On waking 5-7
Rest of the day 4-7

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

When would you consider prescribing Exenatide or Liraglutide? (GLP1 mimetics)

A

Triple therapy has not worked and BMI >35

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

What can cause hypokalaemia

A 
Thiazide and loop
Alkalosis
Cushing'ss
Conns
D&V
Hypomagnesaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

ECG of hypokalaemia

A

Prolonged PR
ST depression
Flat T
U wave

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

Causes of hyperkalaemia

A 
K sparing diuretics, ACE-I, ARB B-blockers, heparin, ciclosporin
Renal failure
Acidosis
Addison's 
Rhabdomyolysis 
Burns 
Blood transfusion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

ECG of hyperkalaemia

A

Flat P
Prolonged PR
Wide QRS
Tall tented T waves (they are higher than R wave)

Eventually sinosoidal and asystole

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

hyperkalaemia management

A 
Calcium gluconate 10% IV
Insulin-dextrose infusion
Nebulised salbutamol 
calcium resonium enema 
haemodialysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

How can you categorise the causes of hyponatraemia? What are the causes within these categories?

A

URINE SODIUM HIGH:
Hypovolaemic = renal loss (diuretics or Addisons)
Euvolemic = SIADH or hypothyroid

URINE SODIUM LOW:
Hypovolaemic = extra renal loss (burns, D&V, sweat)
Hypervolaemic = psychogenic polydypsia or secondary hyperaldosteronism (HF and cirrhosis)

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

How would you manage hyponatraemia?

A

fluid restrict <800ml/day
Hypertonic saline to replace sodium
Conivaptan (causes water loss without electrolytes)

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

What can occur if sodium is replaced too quickly in hyponatraemia?

A

Central pontine demyelination aka locked in

-dysarthria, dysphagia, seizures, paresis

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

What are the causes of hypernatraemia?

A

dehydration
diabetes insipidus
HHS
iatrogenic (drip-arm)

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

What complication can occur if sodium is dropped too quickly in hypernatraemia management?

A

Cerebral oedema

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

What is the management of hypernatraemia?

A

if patient Nathat found in 0.9% saline give 0.9% saline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What are the signs and symptoms of hyperthyroidism?

A 
heat intolerance
thin hair
bulging eyes
facial flushing
weight loss
thin skin 
tachycardic and hypertensive 
amenorrhoea 
diarrhoea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What are the causes of hyperthyroidism?

A 
Grave's disease
De-Quervains (initial hyper phase before hypo)
Iatrogenic - thyroxine, amiodarone 
Toxic multinodular goitre 
Ovarian teratoma (ectopic tissue)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What bloods would suggest hyperthyroidism?

A

low TSH

high T4

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

How can hyperthyroidism be managed?

A

propranolol - symptoms
carbimazole
thyroidectomy

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

What is a thyroid storm? How would it present?

A

hyperthyroid emergency

fever, tachycardia, agitated, D&V, jaundice,

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

How is thyroid storm managed?

A

IV propranolol

Dexamethasone

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

How would subacute thyroiditis (De Quervains) present?

A

Initial short hyperthyroid phase then prolonged hypothyroid
Painful goitre
Raised ESR

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

Compare the goitre of De Quervains subacute thyroiditis and Reidel thyroiditis

A

De Quervains = painful

Reidel = painless, hard, fixed

56
Q

What are the signs and symptoms of hypothyroidism?

A 
cold intolerance
hair loss
thick tongue = slow speech 
brittle nails
weight gain
sluggish/lethargic/tired 
muscle aches and weakness
constipation 
menorrhagia
57
Q

What are the causes of hypothyroidism?

A 
Hashimotos 
Iodine deficiency
De-Quervains
Riedell's 
Lithium 
Hypopituitarism i.e. secondary
58
Q

What bloods would suggest hypothyroidism?

A

raised TSH

low T4

59
Q

What would a low TSH and low T4 suggest?

A

Secondary hypothyroidism due to hypopituitarism

Sick euthyroid

60
Q

How is secondary hypothyroidism managed?

A

MRI pituitary

Steroids prior to giving thyroxine

61
Q

How is hypothyroidism managed?

A

Levothyroxine

62
Q

How does myxoedema present?

A

Bradycardic
Hypothermic
Hypoglycaemic
Hyporeflexic

63
Q

How is myxoedema managed?

A

T3
Hydrocortisone
IV fluids

64
Q

What are the features of thyroid eye disease? Who is it seen in?

A

exophthalmos leading to dry eye
optic disc swelling
ophthalmoplegia

65
Q

How can thyroid eye disease be prevented?

A

Stop smoking

Prednisolone

66
Q

What are complications of thyroid surgery?

A

recurrent laryngeal damage
Swelling and haematoma within a fixed space = airway endangered
parathyroid damage = hypocalcaemia

67
Q

What is the HbA1C target for those with T2 diabetes?

A

On lifestyle or metformin - <48 (6.5%)

On sulfonylureas <53 (7%)

68
Q

What is the management pathway for T2 diabetes?

A 
Tolerate metformin
1 Lifestyle
2 >48 HbA1C - Metformin
3 >58 HbA1C - add 2nd drug
4 remain >58 - add 3rd drug or insulin
5 Insulin therapy

If can’t tolerate metformin then skip this and go to single –> dual –> insulin

69
Q

When is a GLP1 mimetic considered for t2 diabetes?

A

When on dual therapy and:

  • BMI>35 + other condition assoc. with obesity OR
  • BMI <35 but can’t take insulin
70
Q

Which autoantibodies are tested for in thyroid disorderS?

A

Anti TPO - Hashimotos
TSH receptor antibodies - Grave’s
Thyroglobulin antibody

71
Q

How does an addisonian crisis present?

What would a blood gas show?

A

Shock: (tachy, hypotensive, oligouric, weak, LOC)

hyperkalaemia, normal anion gap metabolic acidosis

72
Q

What can precipitate an addisonian crisis?

A

Infection
Trauma
Surgery
Missed medication or withdrawal

73
Q

How is an addisonian crisis managed?

A

100mg hydrocortisone IM/IV

1L Fluids over 30-60 mins (either saline or dex if hypoglycaemic)

Hydrocortisone 6 hourly and then oral after 24hr. Reduce to maintenance dose over 3-4 days

74
Q

What are the signs of Cushing’s syndrome?

A 
Moon face
Personality change
Distended abdomen with striae
Thin skin
GI distress
Thin limbs
Fluid retention
Osteoporosis
Hyperglycaemia

M: gynaecomastia
F: amenorrhoea, hirsutism

75
Q

What causes Cushing’s?

A

Most commonly exogenous corticosteroids

Adrenal tumours

Cushing’s disease - ACTH secreting tumour of pituitary

Ectopic ACTH - small cell lung cancer

Pseudo - excess alcohol or severe depression. Use insulin stress test

76
Q

What would a blood gas show in Cushings?

What is an abnormal result of a low dose dexamethasone suppression test?

How would you interpret the results of a high dose dexamethasone suppression test?

Name another investigation

A

Hypokalaemia metabolic alkalosis
(K particularly low in ectopic ACTH secretion)

LOW DOSE:
normal = cortisol reduces
abnormal = cortisol normal

HIGH DOSE:
cortisol normal but ACTH low = adrenal adenoma
cortisol low but ACTH high = Cushings
cortisol normal but ACTH high = ectopic ACTH

24 hour urinary free cortisol

77
Q

How is Cushing’s syndrome managed?

A

Adrenal - Resection

Cushing’s disease - trans-sphenoidal removal

Ectopic - remove tumour

78
Q

How does Addison’s disease present?

A 
Hyperpigmented skin
Change to body hair distribution
Weight loss
Weak
GI disturbance
Postural hypotension
Hypoglycaemia
79
Q

How is Addison’s diagnosed?

A

Low Na and glucose
High K+ and Ca2+

Short synacthen test - should increase cortisol, if remain low then Addison’s

80
Q

How is Addison’s managed?

A

Hydrocortisone and fludrocortisone

Patient information reg. needles, steroids etc.

81
Q

Which hormones impact serum calcium levels

A

Parathyroid hormone

Calcitriol

82
Q

What are the actions of the parathyroid hormone and where is it secreted?

A

Increase serum calcium and decrease serum phosphate

  • Increase bone Ca resorption
  • Increase kidney Ca reabsorption in DCT –> increase phosphate excretion
  • Increase Ca absorption in GI tract

It also stimulates calcitriol

Secreted from chief cells in parathyroid gland

83
Q

What is calcitriol?

What are the actions of calcitriol and where is it excreted?

A

Calcitriol is activated vit D

Increase serum calcium and serum phosphate:
- Increase Ca and phosphate reabsorption in kidney

84
Q

How does hypercalcaemia present?

A 
Constipation
Renal stones 
Depression
Bone pain
Polyuria and polydipsia
Corneal calcification
Short QT
Hypertension
85
Q

What can cause hypercalcaemia?

A

Main 2:

  • Malignancy - bone mets, myeloma, PTHrP (squamous cell lung cancer)
  • Primary hyperparathyroidism (adenoma)

Others:

  • dehydration
  • sarcoidosis
  • acromegaly
  • thyrotoxicosis
  • thiazides
  • addison’s
86
Q

How is hypercalcaemia managed?

A

FLUIDS - normal saline 3-4L/day
Can use bisphosphonates post rehydration

Others - calcitonin or steroids (sarcoid)
Loop diuretics if can’t tolerate aggressive fluid rehab but caution due to other electrolyte disturbance

87
Q

How does hypocalcaemia present?

A

Trousseau’s sign (carpopedal spasm with BP cuff)
Chvostek’s sign (facial nerve tap = muscles twitch)
Tetany - muscle twitch, spasm, cramp
Perioral paraesthesia
Prolong QT

Chronic - depression and cataracts

88
Q

What is trousseau’s sign?

A

Carpal spasm if brachial artery occluded by inflating BP cuff and maintaining pressure above systolic

  • wrist flexion and fingers drawn together
89
Q

What is chvostek’s sign?

A

Tap parotid cause facial muscles to twitch

90
Q

What causes hypocalcaemia?

A

PHOSPHATE ALSO LOW:
Vit D deficiency
acute pancreatitis

PHOSPHATE RAISED:
CKD
Hypoparathyroidism
Rhabdomyolysis - initial

91
Q

How is hypocalcaemia managed?

A

10ml 10% calcium gluconate
ECG monitoring
Correct cause

92
Q

What happens in primary hyperparathyroidism?

A

Tumour of the parathyroid gland

Elevated PTH –> high Ca and low PO4
Urine calcium:creatinine clearance >0.01

93
Q

How does primary hyperparathyroidism present?

What would you see on x-ray?

A

Can be asymptomatic if mild

Typically elderly female with ++thirst and hypercalcaemia symptoms

Pepperpot skull, generalised osteopenia

94
Q

What happens in secondary hyperparathyroidism?

What is the most common cause?

What blood results do you see?

A

Parathyroid gland hyperplasia due to low serum calcium typically due to CKD

Ca low/normal = Elevated PTH

PO4 high because of raised PTH and due to poor renal excretion

Vitamin D low

95
Q

How does secondary hyperparathyroidism present?

A

Bone and Joint pain

Eventually develop bone disease, osteitis fibrosa cystica and soft tissue calcifications

96
Q

What happens in tertiary hyperparathyroidism?

A

In patients who have secondary hyperparathyroidism due to CKD and subsequently have a renal transplant/dialysis, their PT gland function may not return to normal

PTH high
Ca normal/high
PO4 and vit D low or normal
ALP high

97
Q

What are the features of tertiary hyperparathyroidism?

A

Metastatic calcification
Bone pain ± fracture
Nephrolithiasis
Pancreatitis

98
Q

What are the indications for surgery in primary hyperparathyroidism?

A 
Ca >1mg/dL above normal
Hypercalcuria >400mg/day
Creatinine clearance <30%
Episode of life threatening hypercalcaemia
Nephrolithiasis
Age <50
Neuromuscular symptoms 
Reduction in bone mineral density >2.5SD
99
Q

How is secondary hyperparathyroidism managed?

A

Medical therapy of the cause

Surgery if bone pain, persistent pruritus or soft tissue calcifications

100
Q

How is tertiary hyperparathyroidism managed?

A

Monitor for 12 months

May req. surgery

101
Q

What happens in hypoparathyroidism?

What is a common cause?

How does it present?

What happens in pseudohypoparathyroidism? and what is the resulting biochemistry? How is it diagnosed?

A

Reduced PTH –> low Ca and high PO4
Can be secondary to thyroid surgery
Symptoms of hypocalcaemia

Pseudohypoparathyroidism - target cells insensitive to PTH:
- Low Ca High PO4 high PTH
Diagnosed by measuring urinary cAMP and phosphate following PTH infusion

Pseudopseudohypoparathyroidism is similar to pseudo but normal biochem

102
Q

What presenting features are associated with pseudohypoparathyroidism?

A

Low IQ
Short stature
Shortened 4th and 5th metacarpals

103
Q

What are the types of diabetes insipidus?

A

Central - lack of ADH from post. pituitary

Nephrogenic - kidney unresponsive to ADH

104
Q

What are the features of diabetes insipidus?

A

Polyuria - >3L dilute urine
Polydipsia
Hypernatraemia - lethargy, thirst, weak, irritable

105
Q

How is diabetes insipidus investigated?

A

High plasma osmolality, low urine osmolality

Urine osmolality >700mOsm/kg exclude DI

8 hr water deprivation test - urine should concentrate in normal people

Glucose - rule out DM

106
Q

How is diabetes insipidus managed?

A

Central - desmopressin

Nephrogenic - thiazides, low salt/protein diet

107
Q

What can cause diabetes inspidus?

A

Cranial - idiopathic, post head injury, pituitary tumour or post pituitary surgery, hereditary hemochromatosis

Nephrogenic - genetic, hypercalcaemia, hypokalaemia, lithium

108
Q

What can help you work out if hypoglycaemia is due to endogenous or exogenous insulin?

A

C peptide - only raised if endogenous

109
Q

What is a phaeochromocytoma?

A

Catecholamine secreting tumour
Rule of 10’s:
10% Malignant, 10% extra-adrenal, 10% familial, 10% bilateral

110
Q

How do phaeochromocytoma’s present?

A 
Symptoms are typically episodic: 
Hypertension
Headache
Palpitations
Sweating
Anxiety
111
Q

How is phaeochromocytoma investigated?

A

24 hour urinary metanephrines

CT abdo

112
Q

How is a phaeochromocytoma managed?

A

alpha blockers (phenoxybenzamine) BEFORE beta blockers

Surgical resection

113
Q

Why do you need to ensure hydration and salt is given in phaeochromocytoma?

A

Avoid catecholamine induced volume contraction from unopposed alpha blockage

114
Q

What is Conn’s syndrome?

A

Primary hyperaldosteronism typically due to adrenal adenoma

115
Q

What are the features of Conn’s syndrome?

A

Aldosterone:

  • Sodium and water retention –> hypertension!!
  • Exchange of H+ and Na+ in tubules –> alkalosis
  • Loss of potassium –> Hypokalaemia

Often presents symptomless but can be signs of hypokalaemia

116
Q

What can cause hyperaldosteronism?

A

Primary:

  • Adrenal adenoma
  • Bilateral adrenocortical hyperplasia

Secondary:
- High renin - reduced renal perfusion in renal artery stenosis

117
Q

How is Conn’s syndrome managed?

A

Laparascopic adrenalectomy

Spironolactone post op

118
Q

Which hormones impact prolactin secretion?

A

TRH and Oestrogen stimulate anterior pituitary to release prolactin

Dopamine inhibits secretion

119
Q

What can cause hyperprolactinaemia?

A

Pituitary disturbance
Prolactinoma (pituitary tumour)
Pregnancy/ breast feeding

Drugs:

  • dopamine antagonists (haloperidol, metoclopramide)
  • oestrogens
120
Q

Raised prolactin leads to what further hormone imbalances?

How does hyperprolactinaemia therefore present?

A

Prolactin negatively fees back to inhibit GnRH –> low FSH/LH and testosterone

Females:
- amenorrhoea, galactorrhoea, infertility, decreased libido, dry vagina

Males:
- Reduced facial hair, osteoporosis, galactorrhoea

121
Q

How is hyperprolactinaemia managed?

A

Dopamine agonist - bromocriptine

122
Q

What causes acromegaly?

A

Excess growth hormone due to a pituitary tumour

123
Q

What are the features of acromegaly?

A

Spade like hands
Coarse facial features
Large tongue = interdental spaces and sleep apnoea
Excess sweat and oily skin

Hypopituitarism, headaches, bitemporal hemianopia
Galactorrhoea

124
Q

How is acromegaly diagnosed?

A

Serum IGF1 levels first (also used to monitor disease)

To confirm - oral glucose tolerance test - in normal person, hyperglycaemia inhibit GH but in acromegaly GH levels remain high

Pituitary MRI

125
Q

How is acromegaly managed?

A

Transsphenoidal surgery 1st line

Can try dopamine agonist, GH receptor antagonist, somatostatin agonist

Can try external irradiation - older or failed surgical/medical

126
Q

What are the complications associated with acromegaly?

A

Hypertension
Diabetes
Cardiomyopathy
Colorectal carcinoma

127
Q

How do you differentiate between the primary causes of hyperaldosteronism?

A

CT abdo

Adrenal vein sampling to determine source of increased aldosterone

128
Q

In hyperaldosteronism what would the results of a renin:aldosterone ratio be? Why?

A

raised aldosterone and low renin

Renin is low because of the negative feedback from raised aldosterone = sodium retention

129
Q

Briefly outline the renin-aldosterone-angiotensin feedback loop

A

Renin released when BP drops
converts angiotensinogen –> angiotensin 1
ACE released from lungs
converts angiotensin 1 to angiotensin 2
angiotensin 2 causes vasoconstriction and stimulates release of aldosterone from the adrenals
aldosterone causes sodium and water retention

130
Q

What are the types of pituitary adenoma and how would they present?

A

prolactinoma: amenorrhoea, galactorrhoea
Non-functioning: generalised reduction in hormones
GH secreting: acromegaly
ACTH secreting: cushings

131
Q

What is the most common type of pituitary adenoma

A

prolactinoma

132
Q

What are some generalised symptoms of pituitary adenomas (not related to hormone secretion)

A 
headaches due to dura stretch
bitemporal hemianopia (upper half of vision worse)
133
Q

MEN 1 presents like what and why?

A

parathyroid adenoma = hypercalcaemia
pituitary tumour = prolactinoma
pancreatic tumour = ulcers (as the tumour is often a gastinoma)

134
Q

MEN 2a comprises of what?

A

thyroid carcinoma
pheochromocytoma
parathyroid hyperplasia = hypercalcaemia

135
Q

MEN 2b comprises of what?

A

As 2a (thyroid carcinoma, parathyroid hyperplasia and pheochromocytoma)
+ Marfan appearance
+ mucosa neuromas

136
Q

What is important to be aware of with use of GLP1 analogue’s and DPP4 inhibitors in diabetes management?

A

GLP1 given subcut and can be used with metformin for weight loss

DPP4 doesn’t cause weight gain

Finals (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions