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 hormones are produced by the pituitary gland?

A 
Anterior pituitary:
-prolactin
-TSH
-ACTH
-GH
-FSH
-LH
posterior pituitary:
-oxytocin
-vasopressin (ADH)

connected to the hypothalamus via the pituitary stalk

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

what are the types of hypothyroidism?

A

-primary hypothyroidism- problem with thyroid gland itself
secondary hypothyroidism- usually disorder of the pituitary gland e.g. pituitary apoplexy
congenital hypothyroidism- problem of thyroid dysgenensis or thyroid dyshormogenesis

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

causes of hypothyroidism?

A
  1. hashimoto’s thyroiditis- autoimmune disease associated with T1DM, Addison’s, pernicious anaemia, anti-TPO
  2. Subacute thyroiditis (de Quervain’s)- painful goitre and raised ESR
  3. Post-partum thyroiditis
  4. Riedel thyroiditis
  5. Drugs- lithium, amiodarone
  6. Iron deficiency- most common in developing world
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

causes of thyrotoxicosis?

A
  • Grave’s disease- associated thyroid eye disease, pretibial myxoedema
  • Toxic multinodular goitre- nodules secrete excess thyroid hormones
  • Drugs- amiodarone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

features of hyperthyroidism?

A 
weight loss
manic
heat intolerance
palpitations
sweating
pretibial myxoedema (lateral malleolus)
clubbing
diarrhoea
oligomenorrhagia
anxiety
tremor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

features of hypothyroidism?

A 
weight gain
lethargy
cold intolerance
dry
non-pitting oedema
coarse scalp hair
constipation
menorrhagia
carpal tunnel syndrome
decreased deep tendon reflexes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is subclinical hypothyroidism?

A

high TSH, normal T4 (on the way to developing hypothyroidism)

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

what are the TSH and T4 for poor compliance with thyroxine?

A

high TSH, normal T4

TSH is more representative of long-term thyroid control

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

name some thyroid auto-antibodies?

A

anti-TPO (generally seen in hashimotos thyroiditis)
TSH receptor antibody (seen in grave’s disease)
thyroglobulin antibody

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

tx of hypothyroidism?

A

levothyroxine

SEs- hyperthyroidism, reduced BMD, AF, worsening of angina

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

mx of thyrotoxicosis?

A

propranolol- controls symptoms
carbimazole- reduces thyroid hormone production
radioiodine treatment

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

how does PTH work?

A

bone- increases osteoclast activity= more calcium in bloodstream
kidney- increases vit D activation and calcium resorption from the distal convoluted tubule and increase phosphate excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

how does primary hyperparathyroidism work?

A

seen in elderly females with an unquenchable thirst and raised PTH
most commonly due to a solitary adenoma (80%)
symptoms of hypercalcaemia

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

hormone profile for primary hyperparathyroidism?

A

high PTH
high Ca
low phosphate
urine calcium: creatinine ratio >0.01

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

what is seen on XR of primary hyperparathyroidism?

A

pepperpot skull

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

tx of primary hyperparathyroidism?

A

parathyroidectomy if elevated serum calcium >1mg/dL above normal, hypercalciuria, <50 years, neuromuscular symptoms, osteoporosis

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

what is secondary hyperparathyroidism?

A

parathyroid gland hyperplasia occurs as a result of low calcium, almost always due to chronic renal failure
few symptoms or bone disease and soft tissue calcifications

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

Ix of secondary hyperparathyroidism?

A

high PTH, Ca low or normal, high phosphate, low Vit D

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

tx of secondary hyperparathyroidism?

A

medical therapy usually

surgery if bone pain, pruritic, soft tissue calcifications

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

what is tertiary hyperparathyroidism?

A

ongoing hyperplasia after correction of underlying renal disorder

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

features of tertiary hyperparathyroidism?

A

metastatic calcification
bone pain and/or fracture
nephrolithiasis
pancreatitis

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

ix of tertiary hyperparathyroidism?

A

Can (normal or high), high PTH, phosphate low or normal, vit D normal or low, alk phos high

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

tx of tertiary hyperparathyroidism?

A

allow 12 months to elapse following treatment as many cases will resolve
may need surgery

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

cause of primary hypoparathyroidism?

A

decreased PTH secretion

e.g. secondary to thyroid disease

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

Ix of primary hypoparathyroidism?

A

low calcium, high phosphate

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

features of primary hypoparathyroidism?

A

hypocalcaemia->

  • periorbital paraesthesia
  • trousseau’s sign- carpal spasm after BP cuff
  • chovstek’s sign- tapping over parotid gland causes facial muscles to twitch

if chronic- depression, cataracts
ECH- prolonged QT interval

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

tx of primary hypoparathyroidism?

A

alfacalcidol

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

pseudohypoparathyroidism causes?

A

target cells are insensitive to PTH

due to abnormality in a G protein

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

features of pseudohypoparathyroidism?

A

low IQ, short stature, shortened 4th and 5th metacarpals

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

Ix of pseudohypoparathyroidism?

A

low calcium, high phosphate, high PTH

diagnosis- urinary cAMP and phosphate levels -following an infusion of PTH = pseudo= no rise in either
hypo= both rise

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

what is pseudopseudohypoparathyroidism?

A

pseudohypoparathyroidism with normal biochemistry

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

what acid-base balance is caused by hyperkalaemia?

A

metabolic acidosis
as K+ rises, fewer H+ ions leave bloodstream
They compete with each other for exchange with Na across cell membranes in distal tubule

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

ECG changes of hyperkalaemia?

A

tall-tended T waves
small p waves
widened QRS leading to a sinusoidal pattern and asystole

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

causes of hyperkalaemia?

A 
AKI
metabolic acidosis
addison's disease
rhabdomyolysis
massive blood transfusion
drugs- ACEi, spironolactone, ARBs, ciclosporin, heparin (due to inhibition of aldosterone secretion)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

foods that are high in potassium?

A

salt substitutes, bananas, oranges, kiwi, avocado

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

mx of hyperkalaemia?

A

potassium >7 or ECG changes= URGENT
complication= life-threatening arrhythmias
1. stop precipitating drugs
2. stabilisation of the cardiac membrane- IV calcium gluconate
3. short-term shift in potassium from extracellular to intracellular fluid compartment- combined insulin/dextrose infusion, nebulised salbutamol
4. remove potassium from the body- calcium resonium, loop diuretics, dialysis

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

pathophysiology of hypokalaemia?

A

low K+ in ECF-> water concentration gradient out of cell -> hyperpolarisation of myocyte membrane -> myocyte excitability

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

causes of hypokalaemia?

A

with hypertension:
-cushings, conns, liddle’s syndrome

without hypertension:
-diuretics, GI loss e.g. D&V, renal tubular acidosis, bartter’s syndrome, gitelman syndrome

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

features of hypokalaemia?

A

muscle weakness, hypotonia, predisposition to digoxin toxicity

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

ECG features of hypokalaemia?

A

U waves
small or absent P waves
long QT
long PR

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

tx of hypokalaemia?

A

if severe- IV K+ - transfer to high care area with cardiac monitoring, 3x 1L bags of 0.9% saline with 40mmol KCl per bag over 24 hours

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

causes of hypocalcaemia?

A 
HAVOC
Hypoparathyrodism
Acute pancreatitis
Vitamin D deficiency
Osteomalacia
CKD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

signs and symptoms of hypocalcaemia?

A 
SPASMS
Spasms
Peripheral paraesthesia
Anxious
Seizures
Muscle tone increase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

ix of hypocalcaemia?

A

ECG- long QT interval

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

tx of hypocalcaemia?

A

mild- Adcal

Severe- calcium gluconate

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

causes of primary hyperaldosteronism?

A

bilateral idiopathic adrenal hyperplasia
adrenal adenoma- Conn’s
Adrenal carcinoma- rare

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

features of primary hyperaldosteronism?

A

hypertension
hypokalaemia e.g. muscle weakness
metabolic alkalosis

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

Ix of primary hyperaldosteronism?

A

1st line- plasma aldosterone:renin ratio (high aldosterone and low renin. Negative feedback due to sodium from aldosterone)

high resolution CT abdomen and adrenal vein sampling

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

mx of primary hyperaldosteronism?

A

bilateral adrenocortical hyperplasia: spironolactone (aldosterone antagonist)
adrenal adenoma: surgery

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

what is the hypothalamic-pituitary-adrenal axis?

A

stress-> hypothalamus -> CRH -> pituitary -> ACTH -> adrenal cortex -> cortisol -> mineralocorticoid effects, anti-inflammatory, protein synthesis, lipolysis

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

what is cushing’s syndrome?

A

excess cortisol and loss of HPA axis feedback and loss of circadian rhythm

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

what is cushing’s disease?

A

above caused by a pituitary adenoma

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

causes of cushing’s syndrome?

A

ACTH dependent causes-

  • cushing’s disease- tumour secreted ACTH
  • ectopic ACTH production e.g. SCLC

ACTH independent causes-

  • iatrogenic- steroids
  • adrenal adenoma
  • adrenal carcinoma
  • carney complex: syndrome including cardiac myoxma
  • micronodular adrenal dysplasia
54
Q

what is pseudo-cushings?

A

mimics cushings but due to alcohol excess or severe depression
causes first positive dexamethasone suppression test or 24 hour urinary free cortisol
insulin stress test may be used to differentiate

55
Q

symptoms of cushing’s disease?

A 
personality changes, CNS irritability, hyperglycaemia, moon face
oedema, purple striae
gynaecomastia
increased susceptibility to infections
thin extremities, thin skin
fat deposits on face and back of shoulders
OP
amenorrhora, hirsutism
56
Q

Ix of cushing’s syndrome?

A
  1. overnight dexamethasone suppression test
  2. 24 hr urinary free cortisol
    FBC, U&E
    MRI brain if adenoma suspected
    CT
57
Q

how does a dexamethasone suppression test work?

A

the patient has a dose of dexamethasone (a synthetic glucocorticoid steroid) at night (i.e. 10pm) and their cortisol and ACTH is measured in the morning (i.e. 9am). The intention is the find out whether the dexamethasone suppresses their normal morning spike of cortisol.

if cortisol remains high after low-dose= cushing’s syndrome not due to primary cause e.g. secondary to steroids

if cortisol remains high after low dose but not high dose= cushing’s disease

if cortisol not suppressed by either= ectopic ACTH e.g. lung cancer or adrenal adenoma producing cortisol

58
Q

tx of cushing’s syndrome?

A

if iatrogenic- stop steroids
cushing’s disease- remove pituitary adenoma
remove adrenal adenoma
ectopic ACTH- remove tumour

59
Q

hormone production of adrenal gland?

A
  1. medulla- produces catecholamines and adrenaline
  2. cortex-
    - glucocorticoids- cortisol
    - mineralocorticoids- aldosterone
    - gonadocorticoids- androgens
60
Q

what is addison’s disease?

A

autoimmune destruction of adrenal glands

61
Q

other causes of destruction of adrenal glands?

A

TB, mets, HIV, antiphospholipid syndrome, pituitary disorders, exogenous glucocorticoid therapy

62
Q

features of addison’s disease?

A 
lethargy
weakness
anorexia
N&amp;V
weight loss
salt-craving
hyperpigmentation- esp palmar creases, vitiligo, hypotension, hypoglycaemia
63
Q

electrolyte abnormalities of addisons?

A

low Na and high K

64
Q

features of addisons crisis?

A

collapse, shock, pyrexia

65
Q

Ix of addison’s disease?

A

-ACTH stimulation test (short synacthen test)
plasma cortisol measured-> given IM synacthen 250ug -> cortisol measured 30 mins after

-in primary care, do 9am cortisol
100-500= prompts ACTH stimulation test

66
Q

tx of addison’s diaease?

A

replace glucocorticoids- hydrocortisone

replace mineralocorticoids- fludrocortisone (isn’t required in an Addisonian crisis)

67
Q

what is acromegaly?

A

excess growth hormone secretion

68
Q

causes of acromegaly?

A

pituitary adenoma
ectopic GHRH
GH production by tumours e.g. pancreatic

69
Q

features of acromegaly?

A

coarse facial appearance, spade-like hands, increased feet size
large tongue, prognathism, interdental spaces
sweat gland hypertrophy- excessive sweating and oily skin
features of pituitary tumour- hypopituitarism, headaches, bitemporal hemianopia
raised prolactin in 1/3 of cases-> galactorrhoea
6% have MEN 1

70
Q

complications of acromegaly?

A

hypertension
diabetes
cardiomyopathy
colorectal cancer

71
Q

Ix of acromegaly?

A

GH levels not reliable on their own
IGF-1 levels
oral glucose load-> lack of suppression of GH to <1ug/L
pituitary MRI-> pituitary adenoma

72
Q

tx of acromegaly?

A

trans-sphenoidal surgery- remove adenoma
DA agonists- bromocriptine
Somatostatin analogue- directly inhibit the release of GH e.g. octreotide
GH receptor antagonist e.g. pegvisomant

73
Q

what is diabetes insipidus?

A

a condition characterised by either a deficiency of anti-diuretic hormone, ADH (cranial DI) OR an insensitivity to ADH (nephrogenic DI)

74
Q

causes of cranial DI?

A 
Idiopathic
post-head injury
pituitary surgery
craniopharyngiomas
DIDMOAD
haemochromatosis
75
Q

causes of nephrogenic DI?

A

Genetics- affects vasopressin receptor
hypercalcaemia, hypokalaemia
demeclocycline, lithium
tubulo-interstitial disease: obstruction, sickle-cell, pyelonephritis

76
Q

features of DI?

A

polyuria, polydipsia

77
Q

Ix of DI?

A

High plasma osmolality
low urine osmolality- >700 excludes DI
water deprivation test

78
Q

mx of DI?

A

Nephrogenic- thiazides, low salt/protein diet

Central- desmopressin

79
Q

how does vasopressin (ADH) work?

A

V1- blood vessels (constriction)- increases arterial pressure
V2- kidneys (fluid reabsorption)- increases arterial pressue

80
Q

what causes T2DM?

A

A relative deficiency of insulin due to an excess in adipose tissue

81
Q

symptoms of T1DM and T2DM?

A

T1DM- weight loss, polydispia, polyuria, DKA- vomiting, abdo pain, reduced consciousness level
T2DM- often picked up incidentally on routine bloods cells, polyuria, polydipsia

82
Q

diagnosis of diabetes?

A

if the patient is symptomatic only one of the following, if asymptomatic must be demonstrated twice-

  • fasting glucose >7mmol/L
  • random glucose >11.1mmol/L

HbA1C- glycosylated Hb
>6.5% (48mmol/mol)= diagnostic
false positives for increased red cell turnover e.g. haemolytic anaemia, HIV

83
Q

what is pre-diabetes?

A

HbA1C 42-47
or fasting glucose 6.1-6.9
also called impaired fasting glucose

84
Q

what is impaired glucose tolerance?

A

fasting glucose <7 and OGTT 2-hour value >7.8mmol/L but less than 11.1mmol/L

85
Q

mx of T1DM?

A

HbA1c monitored every 3-6 months target of <48
blood glucose
insulin- long-acting e.g. insulin detemir
self-testing at least 4 times a day, more frequent monitoring during periods of illness, before,during and after sport
metformin- add if BMI >25

86
Q

mx of T2DM?

A 
1st line= metformin 
if HbA1c >58mmol/mol, add 1 of:
-gliptin
-sulphonylurea
-pioglitazone
-SGLT-2 inhibitor

if HbA1c continues to remain >58-

  • insulin or
  • metformin and sulphonylurea and 1 of:
  • gliptin
  • pioglitazone
  • SGLT-2 inhibitor

if triple therapy not tolerated, CI’d or not effective AND BMI >35-> metformin, sulphonylurea and GLP-1 mimetic

87
Q

lifestyle advice for T2DM?

A

diet and exercise
BP target <140/80
statin if QRISK2 >10%

88
Q

what to give if metformin CI’d for T2DM?

A

gliptin OR
sulphonylurea OR
pioglitazone

89
Q

meds for diabetic neuropathy and N&V?

A

neuropathy- amitriptyline, duloxetine

N&V- metoclopramide

90
Q

SEs of insulin?

A

hypoglycaemia
weight gain
lipodystrophy

91
Q

how does metformin work?

SEs, CIs and positives?

A

increases insulin sensitivity and decreases hepatic gluconeogenesis
SE- GI upset, lactic acidosis, CI- eGFR <30ml/min
positives- can cause weight loss

92
Q

examples, mechanism, SEs and CI of sulphonylureas?

A

e.g. gliclazide
stimulates pancreatic beta cells to secrete insulin
SE- hypoglycaemia, weight gain, hyponatraemia
CI- pregnancy and breastfeeding- causes neonatal hypoglycaemia

93
Q

examples, mechanism, SE and CI of glitazones?

A

pioglitazone
activates PPAR-gamma receptor in adipocytes to promote adipogenesis andfatty acid uptake
SE- weight gain, fluid retention, fractures
CI- heart failure

94
Q

examples, SE and positives of DPP4 inhibitors?

A 
e.g. gliptins
increases incretin levels which inhibits
glucagon secretion
SE- pancreatitis
positive- no weight changes
95
Q

example, SE and positive of SGLT-2 inhibitors?

A

e.g. glifozins
inhibits resorption of glucose in the kidney
SE- UTI, DKA
positives- typically results in weight loss

96
Q

pathophysiology of DKA?

A

caused by uncontrolled liplysis which results in an excess of free fatty acids that are ultimately converted to ketone bodies

97
Q

precipitating features of DKA?

A

Infection
MI
missed insulin doses

98
Q

features of DKA?

A

abdo pain
polyuria, polydipsia, dehydration
Kussmaul respiration (deep hyperventilation)
Acetone-smelling breath (‘pear drop’ breath)

99
Q

diagnostic criteria for DKA?

A

Glucose >11mmol/L or known DM
pH <7.3
BICARB <15
ketones >3 or urine ketones ++ on dipstick

100
Q

mx of DKA?

A
  1. Fluid replacement- 0.9% saline 1L in first hour then 0.9% saline and KCl over 2 hours and continued with increased time intervals
    (slower in 15-25y/o due to risk of cerebral oedema)
  2. Insulin- IV .1 unit/kg/hour
  3. Once BG is <15mmol/l start 5% dextrose infusion
  4. Correction of hypokalaemia if 3.5-5.5 (senior review if lower)
  5. Continue with long-acting insulin
101
Q

complication of DKA?

A 
gastric stasis
VTE
arrhythmias
cerebral oedema
ARDs
AKI
102
Q

what is hyperosmolar hyperglycaemic state?

A

hyperglycaemia in T2DM-> resulting in osmotic diuresis, severe dehydration and electrolyte deficiencies
-typically presents in the elderly

103
Q

clinical features of hyperosmolar hyperglycaemic state?

A

onset in slower than T2DM (over days) and therefore dehydration and metabolic disturbances are worse
fatigue- lethargy, N&V
neuro- decreased consciousness, headaches, papilloedema, weakness
haem- hyperviscosity- increased risk of VTE, stroke
CV- dehydration, hypotension, tachycardia

104
Q

diagnosis of hyperosmolar hyperglycaemic state?

A
  1. hypovolaemia
  2. marked hyperglycaemia (>30mmol/L) without sigf ketonuria or acidosis
  3. Significantly raised serum osmolarity (>320mosmol/kg)
    - 2Na + glucose + urea
105
Q

mx of hyperosmolar hyperglycaemic state?

A
  1. normalise the osmolality
  2. replace fluid and electrolyte imbalance
  3. normalise blood glucose
106
Q

most common type of pituitary adenoma?

A

prolactinomas

107
Q

symptoms of pituitary adenoma?

A

excess hormone e.g. cushings
depletion of hormone
stretching of dura around pituitary fossa -> headache
compression of optic chiasm -> bitemporal hemianopia

108
Q

Ix of pituitary adenoma?

A

pituitary bloods- GH, prolactin, ACTH, TFT, FSH/LH
visual field testing
MRI

109
Q

mx of pituitary adenoma?

A

hormonal therapy (e.g. bromocriptine for prolactinomas), surgery

110
Q

what is MEN type 1?

A
  • parathyroid (95%)- hyperparathyroidism due to parathyroid hyperplasia
  • pituitary (70%)
  • pancreas (50%) e.g. insulinoma, gastrinoma (leading to recurrent peptic ulceration)
111
Q

what is MEN type 2?

A

medullary thyroid cancer e.g. phaeochromocytoma

112
Q

what is the most common drug cause of gynaecomastia?

A

spirinolactone

113
Q

symptoms of addisonian crisis?

A

hypovolaemia
hyponatraemia
hyperkalaemia

114
Q

causes of addisonian crisis?

A

sepsis or surgery causing an acute exacerbation of chronic insufficiency (Addison’s, Hypopituitarism)
adrenal haemorrhage eg Waterhouse-Friderichsen syndrome (fulminant meningococcemia)
steroid withdrawal

115
Q

mx of addisonian crisis?

A

hydrocortisone 100 mg im or iv
1 litre normal saline infused over 30-60 mins or with dextrose if hypoglycaemic
continue hydrocortisone 6 hourly until the patient is stable. No fludrocortisone is required because high cortisol exerts weak mineralocorticoid action
oral replacement may begin after 24 hours and be reduced to maintenance over 3-4 days

116
Q

what is the most common presentation for MEN 1?

A

Hypercalcaemia

117
Q

2 tests to confirm cushing’s syndrome?

A

overnight dexamethasone suppression test (most sensitive)

24 hr urinary free cortisol

118
Q

what to do in a hypoglycaemic attack with impaired GCS?

A

give IV glucose if there is IV access

if GCS not impaired, give quick-acting carbohydrate such as GlucoGel®

119
Q

causes of raised prolactin?

A 
prolactinoma
pregnancy
oestrogens
physiological: stress, exercise, sleep
acromegaly: 1/3 of patients
polycystic ovarian syndrome
primary hypothyroidism
120
Q

rules of radioactive iodine?

A

Involves drinking a single dose of radioactive iodine
This is taken up by the thyroid, and the emitted radiation destroys a portion of the thyroid cells
Patients can be left hypothyroid afterwards and require levothyroxine replacement

There are rules regarding:
Not pregnant or allowed to get pregnant within 6 months
Avoiding contact with children and pregnant women
Limiting contact with others for several days after receiving the dose

121
Q

What cells secrete PTH?

A

chief cells

122
Q

how to investigate pheochromocytoma?

adrenal tumour

A

plasma metanephrines or 24 hour urine catecholamines (both breakdown products of adrenalin).

123
Q

mx of acromegaly?

A

Both somatostatin analogues (e.g. ocreotide) and dopamine agonists (e.g. bromocriptine)

124
Q

causes of SIADH?

A

Post-operative from major surgery
Infection, particularly atypical pneumonia and lung abscesses
Head injury
Medications (thiazide diuretics, carbamazepine, vincristine, cyclophosphamide, antipsychotics, SSRIs, NSAIDSs,)
Malignancy, particularly small cell lung cancer
Meningitis

125
Q

electrolyte abnormality of SIADH?

A

hyponatraemia (dilutional)

Clinical examination will show euvolaemia

126
Q

mx of SIADH?

A

Fluid restriction

vaptans (ADH receptor blockers such as tolvaptan).

127
Q

risk of rapid correction of hyponatraemia?

A

A rise in sodium that is too fast gives a risk of central pontine myelinolysis (a neurological condition).

128
Q

antibodies in thyroid disease?

A

anti-TPO- Grave’s Disease and Hashimoto’s Thyroiditis
Antithyroglobulin Antibodies- Grave’s Disease, Hashimoto’s Thyroiditis and thyroid cancer.
TSH Receptor Antibodies- graves

129
Q

what is levothyroxine?

A

synthetic T4 and metabolises to T3 in the body.

130
Q

what causes pretibial myxoedema?

A

a reaction to the TSH receptor antibodies- there are deposits of mucin under the skin on the anterior aspect of the leg

131
Q

what is De Quervain’s Thyroiditis?

A

De Quervain’s Thyroiditis describes the presentation of a viral infection with fever, neck pain and tenderness, dysphagia and features of hyperthyroidism. There is a hyperthyroid phase followed by hypothyroid phase as the TSH level falls due to negative feedback.

finals (14 decks)

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