Brainscape's Knowledge GenomeTM

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


See full index

Phase 2a > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What’s the difference between endocrine and exocrine?

A

endocrine- glands pour secretions into bloodstream
exocrine- glands pour secretions though a duct to site of action

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

What happens to TSH if you remove the thyroid/ thyroid is under active?

A

TSH will increase/ be elevated

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

What happens to TSH if you have an overactive thyroid?

A

TSH decreased

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

What happens to FSH and LH after menopause?

A

increases

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

What are the diseases of the pituitary?

A

benign pituitary adenoma
craniopharygioma
trauma
apoplexy/ sheehans (bleeding)
sarcoid/ TB

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

How big is the pituitary?

A

1cm in diameter

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

How do pituitary tumours present?

A
  1. PRESSIRE OF LOCAL STRUCTURE
    bitemporal hemianopia (double vision)
    headache
    CSF leakage
  2. PRESSURE ON NORMAL PITUITARY
    hypopituitarism
  3. FUNCTIONING TUMOUR
    prolactinoma
    acromegaly and gigantism
    Cushing’s disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is Cushing’s disease?

A

too much cortisol

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

What is acromegaly?

A

too much growth hormone

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

How do you tell the difference between CSF leakage from nose and snot?

A

CSF has glucose in it

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

How does somebody with a hypopituitary present?

A

pale
no body hair
central obesity

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

What happens if you have excess GH as a child? Why only in a child?

A

gigantism

tumour on pituitary presses on it and causes hypothyroidism meaning that the child won’t go through puberty (no testosterone secretion, etc)

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

How does acromegaly present?

A

big hands
big jaw
excess sweating
big heart

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

What is galactorrhea?

A

a milky nipple discharge unrelated to the normal milk production of breast-feeding

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

Can both men and women get prolactinomas?

A

Yes

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

Symptoms of prolactinomas?

A

galactorrhea
infertility
loss of libido
visual field defect

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

How quickly does acromegaly progress?

A

slow onset

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

Symptoms of Cushing’s?

A

main symptoms is weight gain, ulcers, stretch marks, easy bruising

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

What does an orchidometer measure?

A

testicular volume in mL

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

What is normal pre-pubertal testicular volume?

A

1-3 mL

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

What is normal testicular volume for an adult male?

A

15-25mL

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

What is thelarche?

A

breast development signalling first visible change of puberty

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

What induces thelarche?

A

oestrogen

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

How long do thelarche last?

A

3 years approx

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

What are you looking for on a pelvic ultrasound?

A

check for mullerian structures
morphology of uterus
morphology of ovaries

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

What are mullerian structures?

A

structures found in the female fetus that eventually develop into a woman’s reproductive organs

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

What causes growth of pubic and axillary hair in girls?

A

adrenal androgens and ovarian androgens

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

What is adrenarche?

A

maturation of adrenal glands, zona reticularis is formed

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

What happens if adrenarche happens in children?

A

mild advanced bone age
axillary hair
oily skin
mild acne
body odour

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

Which children most commonly experience adrenarche?

A

obese children

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

What is the name for early puberty?

A

precocious puberty

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

What are the types of precocious puberty?

A

true precocious puberty
precocious pseudopuberty

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

What is the gender distribution of true precocious puberty?

A

90% female
10% male

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

Why is it alarming if a male child has true precocious puberty?

A

he is likely to have a brain tumour

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

How do you differentiate between diagnosis of true precocious puberty and precocious pseudopuberty?

A

GnRH (LHRH) test

inject GnRH

If amount of of FSH and LH rises - true precocious puberty

If amount of TSH and LH stays the same - precocious pseudopuberty

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

What is the treatment for precocious puberty?

A

GnRH superagonist to suppress pulsatility of GnRH secretion

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

In what percentage of children does delayed puberty occur?

A

3% of children

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

What are the effects of delayed puberty?

A

psychological problems
defects in reproduction
reduced peak bone mass
delay in acquisition of sex characteristics

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

What’s the average size for an adult penis?

A

12-14cm

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

What is CDGP?

A

constitutional delay of growth and puberty

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

What is the most common cause of delayed puberty?

A

CDGP

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

What are the hormones of the anterior pituitary?

A

adrenocorticotrophic hormone (ACTH)
thyroid-stimulating hormone (TSH)
luteinising hormone (LH)
follicle-stimulating hormone (FSH)
prolactin (PRL)
growth hormone (GH)
melanocyte-stimulating hormone (MSH)

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

What are the hormones of the posterior pituitary?

A

anti-diuretic hormones (ADH)
oxytocin

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

What are the possible co-morbidities associated with acromegaly?

A

arthritis
headache
arthritis
insulin-resistant diabetes
sleep apnoea
hypertension
heart disease

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

How does acromegaly affect life expectancy?

A

reduces average life expectancy by approx 10 years

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

What is the difference in the way water-soluble and fat-soluble hormones interact with the cell?

A

water-soluble hormones bind to a surface receptor, fat-soluble hormones diffuse into the cell

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

Whats the difference in half-life of water-soluble and fat soluble hormones?

A

water-soluble: short half life
fat-soluble: long half life

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

Whats the difference in transport of water-soluble and fat soluble hormones?

A

water-soluble: unbound
fat-soluble: protein bound

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

Whats the difference in clearance of water-soluble and fat soluble hormones?

A

water-soluble: fast
fat-soluble: slow

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

What is the difference in the water peptides/ monoamine hormones are stored vs steroids?

A

peptides/ monoamines- stored in vesicles
steroids- synthesised on demand

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

What is paracrine?

A

cellular secretions/ signals that act on adjacent cells

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

What is autocrine?

A

cellular signals/ secretions that feedback on the same cell that created the hormones

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

How big are peptide hormones?

A

variable- 3 to 180 amino acids

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

What type of hormone is insulin?

A

peptide

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

How does insulin exert its effect?

A
  • insulin binds to receptor
  • causes phosphorylation of intracellular tyrosine residues associated with the receptor
  • this offsets the tyrosine kinase signal transduction pathway inside cell
  • leads to decreased plasma glucose
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

By what mechanisms does the action of insulin decrease blood glucose?

A
  • translocation of glut-4 transporter to plasma membrane and influx of glucose
  • glycogen synthesis in the liver
    -glycolysis
  • fatty acid synthesis in liver and adipose tissue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What are catecholamines?

A

type of neurohormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What are the catecholamines and where are they secreted from?

A

adrenaline and noradrenaline: adrenal medulla
dopamine: hypothalamus

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

What are the catecholamines and where are they secreted from?

A

adrenaline and noradrenaline: adrenal medulla
dopamine: hypothalamus

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

What receptors do adrenaline and noradrenaline act upon?

A

adrenoreceptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What are the two lodothyronines?

A

tyroxine (T4) and triiodothyronine (T3)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What are the two lodothyronines?

A

tyroxine (T4) and triiodothyronine (T3)

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

Where is T4 produced?

A

thyroid gland

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

Where is T3 produced?

A

20% of T3 in circulation is secreted directly by thyroid gland, other 80% is T4 that has been converted to T3 after it leaves the thyroid gland

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

What enzyme converts T4 to T3?

A

iodothyronine deiodinase

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

What are the two classes of steroid hormones?

A

corticosteroids
sex (gonadal) steroids

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

What are the classes of corticosteroids?

A

glucocorticoids
mineralocorticoids

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

What are the classes of sex steroid?

A

androgens
oestrogens
progestogens

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

What are steroid hormones derived from?

A

cholesterol

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

How is cholesterol converted to each steroid hormone?

A
  • cholesterol converted to pregnenolone
  • pregnenolone converted to progesterone
  • progesterone converted to cortisol in the adrenal glands
  • progesterone converted to androstenedione then to testosterone in the ovaries or testes
  • testosterone converted to estradiol in the ovaries
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

How are steroid hormones transported around the body?

A

vitamine D binding protein

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

Where is glucose stored?

A

liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What do muscles use for fuel?

A

free fatty acids

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

What happens if glucose gets too high?

A
  1. inhibition of glucagon secretion
  2. stimulation of insulin release
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Where is insulin and glucagon secreted?

A

islets of langerhans in the pancreas
insulin- beta cells
glucagon- alpha cells

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

Why is it getting more difficult to differentiate between T1 and T2 diabetes?

A

Because of increased levels of obesity, T2DM is being diagnosed in younger patients including children

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

What are microvascular complications of T1DM?

A

In UK, 30% of T1DM patients will develop diabetic nephropathy

Nephropathy tends to lead to retinopathy and severe neuropathy which massively affects quality of life

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

What is nephropathy?

A

deterioration of kidney function
can end up in kidney failure (end stage renal disease)

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

Define type 1 diabetes mellitus

A

autoimmune destruction of pancreatic beta cells leading to complete insulin deficiency

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

When do T1DM usually present?

A

age 5-15

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

What percentage of diabetes is T1DM?

A

10%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What is glycosuria?

A

sugar in the urine

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

What are the risk factors for T1DM?

A

Northern European
Autoimmune disease
Family History

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

What are the signs and symptoms of T1DM?

A
  • “classic triad”: polydipsia, polyruria, weightloss (BMI < 25)
  • short history of severe symptoms
  • possibly presents with ketosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What is the name for extreme thirstiness?

A

polydipsia

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

What is the name for frequent urination?

A

polyuria

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

How is T1DM diagnosed?

A

Either:
- fasting glucose >= 7.0 mmol/L
- random glucose >= 11.0 mmol/L
- HbA1c >= 6.5% (48 mmol/mol)

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

What is important to remember about diagnosing diabetes using HbA1c?

A

a value less that 6.5% DOES NOT exclude diabetes as this test is not as sensitive as fasting samples in detecting diabetes

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

What is the treatment for T1DM?

A

insulin, short or long acting

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

How long does short and long acting insulin work for?

A

short: 4-6 hrs
long: 12-24 hrs

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

Which antibodies can you check for in T1DM?

A

Anti GAD
pancreatic islet cell Ab
islet antigen-2 Ab
ZnT8

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

Why does T2DM occur?

A

patients gradually become insulin resistant AND/OR beta cells fail to secrete enough insulin

non-insulin dependent and progresses from impaired glucose tolerance

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

What causes T2DM?

A
  • reduced insulin secretion/ increased insulin resistance
  • gestational diabetes
  • steroids
  • Cushing’s
  • chronic pancreatitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What are the risk factors of T2DM?

A
  • lifestyle: obesity, inactivity, calorie and alcohol excess
  • higher prevalence in asian men
  • > 40yrs age
  • hypertension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What are the signs and symptoms of T2DM?

A

polydipsia
polyuria
glycosuria
central obesity
slower onset
blurred vision

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

What are the investigations for T2DM?

A

Exactly the same as type 1:

Either:
- fasting glucose >= 7.0 mmol/L
- random glucose >= 11.0 mmol/L
- HbA1c >= 6.5% (48 mmol/mol)

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

Describe first line management of T2DM

A

1st line- lifestyle changes
- dietary advice (high complex carbs, low fat)
- smoking cessation
- decrease alcohol intake
- encourage exercise
- regular blood glucose and HbA1c monitoring

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

Describe second line management of T2DM

A

2nd line- medication

  1. METFORMIN (e.g. biguanide)
  2. If HbA1c remains high then DUAL THERAPY with metformin:
    - DPP4 inhibitor
    - Sulphonylurea (e.g. gliclazide)
    - pioglitazone
  3. If still high = TRIPLE THERAPY with metformin
  4. Insulin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

How does metformin work and what type of patients suit it best?

A

increases sensitivity to insulin, decreases hepatic gluconeogenesis

first choice in overweight patients as it can cause a slight weight decrease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

How does sulphonylurea treat T2DM?

A

increases insulin secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

What are the notable side effects of metformin?

A

gastrointestinal upset
lactic acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Why is sulphonylurea becoming less popular as a 2nd line treatment for T2DM?

A

causes weight gain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

What are the notable side effects of sulphonylurea?

A

hypoglycaemia
weight gain
hyponatraemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Give 2 examples of sulphonylureas

A

gliclazide
glimepiride

104
Q

What is DKA?

A

diabetic ketoacidosis- complete lack on insulin resulting in ketone production

105
Q

What causes DKA?

A

unrelated/ undiagnosed type 1 diabetes
infection/ illness

106
Q

Describe the pathophysiology of DKA

A
  1. absence of insulin causes hyperglycaemia and increased ketones
  2. hyperglycaemia causes osmotic diuresis- dehydration
  3. glucose and ketones escape in urine
  4. circulating ketones are acidic and cause acidosis
107
Q

What is the direct effect of ketones on the body?

A

anorexia and vomiting

108
Q

What are the signs and symptoms of diabetic ketoacidosis?

A

extreme diabetes symptoms plus:
nausea and vomiting
weight loss
confusion and reduced mental state
lethargy
abdominal pain
Kussmaul’s breathing
‘pear drop’ breath
hypotension
tachycardia

109
Q

What is kussmaul’s breathing?

A

fast, deep breaths that occur in response to metabolic acidosis

110
Q

What investigations can be done to confirm diabetic ketoacidosis?

A
  • random plasma glucose > 11mmol/L
  • plasma ketones >3mmol/L
  • blood pH <7.35, or bicarb <15mmol/L
  • urine dipstick: glycosuria, ketonuria
  • serum U+E:
    -raised urea and creatinine
    -decreased total K+, increased serum K+
111
Q

What is the treatment for diabetic ketoacidosis?

A
  1. ABC management
  2. replace fluid- 0.9% saline IV
  3. IV insulin
  4. restore electrolytes (e.g. K+)
112
Q

What is HHS?

A

hyperosmolar hyperglycaemic state

113
Q

What causes HHS?

A

untreated/ undiagnosed T2DM
infection/ illness

114
Q

What are the signs and symptoms of HHS?

A

extreme diabetes symptoms plus:
confusions and reduced mental state
lethargy
severe dehydration

115
Q

What investigations confirm a diagnosis of HHS?

A
  • random plasma glucose > 11mmol/L
  • urine dipstick: glycosuria
  • high plasma osmolality
  • U+E
    • decreased total body K+
    • increased serum K+
116
Q

What is the treatment for HHS?

A
  • replace fluid- 0.9% saline
  • insulin- AT LOW RATE OF INFUSION
  • restore electrolytes
  • low molecular weight heparin (LMWH)
117
Q

Why must patients with HHS be given insulin at a low rate of infusion?

A

patients with HHS have a high sensitivity to insulin

requires a low infusion rate to prevent cerebral oedema caused by glucose being lowered too quickly

118
Q

What is hypoglycaemia?

A

low plasma glucose causing impaired brain function

119
Q

What is neutropenia?

A

abnormally low concentration of neutrophils

120
Q

What glucose value signals hypoglycaemia?

A

3.9 mmol/L

121
Q

What is hyperthyroidism?

A

clinical effects of too much thyroid hormone

122
Q

What is the difference between primary and secondary hyperthyroidism?

A

primary- abnormal increased thyroid function
secondary- abnormal increased TSH production

123
Q

What are the causes of hyperthyroidism?

A
  • 65-75% caused by GRAVES DISEASE
  • toxic multi nodular goitre
  • toxic adenoma
  • metastatic follicular thyroid cancer
  • iodine excess

secondary cause: TSH secreting pituitary tumour

124
Q

What is the ratio of F:M diagnosed with Graves disease?

A

9:1

125
Q

Who is affected by hyperthyroidism?

A

mostly young women aged 20-40

126
Q

What are the risk factors for hyperthyroidism?

A

smoking
stress
HLA-DR3
other autoimmune diseases (T1DM, Addisons, vitiligo)

127
Q

What are the signs and symptoms of hyperthyroidism?

A

hot and sweaty
diarrhoea
hyperphagia
weight loss
palpitations
tremor
irritability
anxiety/ restlessness
oligomenorrhoea
goitre

128
Q

What is goitre?

A

swelling of thyroid gland causing lump in the front of the neck

129
Q

What is hyperphagia?

A

abnormally big desire for food/ excessive eating

130
Q

What is oligomenorrhoea?

A

abnormal menstruation involving infrequent periods

131
Q

Which investigations confirm a diagnosis of hyperthyroidism?

A
  • Thyroid function tests (TFTs) showing increased T4/ T3, plus:

primary: decreased TSH
secondary: increased TSH

  • Thyroid autoantibodies (anti-TSHR)
  • ultrasound and CT head
132
Q

What is the treatment for hyperthyroidism?

A
  1. DRUG MANAGEMENT
    a) beta blockers (rapid symptom relief)
    b) 1st line: carbimazole
    c) 2nd line: propylthiouracil
  2. RADIOIODIDE
  3. TYROIDECTOMY
133
Q

How does carbimazole and propylthiouracil treat hyperthyroidism?

A

carbimazole- blocks synthesis of T4

propylthiouracil- prevents T4 to T3 conversion

134
Q

What are the consequences of untreated hyperthyroidism during pregnancy?

A
  • intrauterine growth resistance (IUGR)
  • pre eclampsia
  • preterm delivery
  • risk of stillbirth/ miscarriage
135
Q

How does Graves disease cause hyperthyroidism?

A

IgG antibodies bind to TSH receptors to increase T4/ T3 production

136
Q

What are the symptoms of Graves disease?

A

hyperthyroidism symptoms plus:
- thyroid eye disease
- pretibial myxoedema
- thyroid acropachy

137
Q

What are the features of thyroid eye disease?

A

eye retraction
periorbital swelling
proptosis/ exophthalmos (bulging eyeballs)

138
Q

What percentage of patients with Graves disease have thyroid eye disease?

A

25-50%

139
Q

How does thyroid acropachy present?

A

clubbing
painful finger and toe swelling
periosteal reaction (bone growth)

140
Q

What is hypothyroidism?

A

clinical effects of lack of thyroid hormone

141
Q

What is the difference between primary and secondary hypothyroidism?

A

primary: abnormally low thyroid function

secondary: abnormally low TSH production

142
Q

What are the causes of hypothyroidism?

A
  1. AUTOIMMUNE: Hashimotos inflammation = goitre), Primary atrophic hypothyroidism (atrophy = no goitre)
  2. OTHER PRIMARY: iodine deficiency, drugs (antithyroid drugs, iodine, lithium), post thyroidectomy/ radio iodine)
  3. SECONDARY: hypopituitarism
143
Q

How many people are diagnosed with hypothyroidism every year?

A

4 in every 1000 people

144
Q

Who is most commonly affected by hypothyroidism?

A

affects F:M in a ratio of 6:1
mainly > 40 yrs old

145
Q

What are the signs and symptoms of hypothyroidism?

A

fatigue
weight gain
loss of appetite
cold
lethargy
constipation
low mood/ depression
menorrhagia
goitre

146
Q

What is the treatment for hypothyroidism?

A

levothyroxine (T4)

147
Q

List the hormones of the anterior pituitary

A
  • adrenocorticotropic hormone (ACTH)
  • growth hormone (GH)
  • luteinising hormone (LH)
  • follicle-stimulating hormone (FSH)
  • prolactin
  • thyroid-stimulating hormone (TSH)
148
Q

List the hormones of the posterior pituitary

A
  • anti-diuretic hormone (ADH)
  • oxytocin
149
Q

Where is melanocyte-stimulating hormone produced and what does It do?

A

pars intima- part of pituitary between anterior and posterior

acts on cells in skin to stimulate production of melanin (pigment which prevents against UV radiation)

150
Q

Where are the hormones released from the posterior pituitary produced?

A

hypothalamus

151
Q

What is another name for ADH?

A

vasopressin

152
Q

What does ACTH do?

A

stimulates adrenal glands to secrete steroids (e.g. cortisol)

153
Q

What does GH do?

A

regulates growth, metabolism and body composition by acting on liver, bones, adipose tissue and muscles

154
Q

What does LH and FSH do? What are they collectively called?

A

gonadotrophins

act on ovaries/ testes to stimulate sex hormone production and egg/ sperm maturity

155
Q

What does prolactin do?

A

stimulates milk production in mammary glands

156
Q

What does TSH do?

A

stimulates thyroid gland to secrete thyroid hormone

157
Q

What does ADH/ vasopressin do?

A

controls water balance and blood pressure

158
Q

What does oxytocin do?

A

stimulates uterine contractions during labour and milk secretion during breast feeding

159
Q

What is Cushing’s syndrome?

A

long term exposure to excessive cortisol hormone released by adrenal glands

160
Q

What is the difference between a syndrome and a disease?

A

A disease typically has a defining cause, distinguishing symptoms and treatments. A syndrome is a group of symptoms that may not have a definite cause.

161
Q

What are the two types of causes of Cushing’s syndrome

A

ACTH dependent and ACTH independent

162
Q

What is the difference between Cushing’s syndrome and Cushing’s disease?

A

Cushing’s disease is a specific type of Cushing’s syndrome resulting from a pituitary tumour

163
Q

What are the ACTH dependent causes of Cushing’s syndrome?

A
  • Cushing’s disease- ACTH secreting from pituitary adenoma
  • Ectopic ACTH production from small cell lung cancer
164
Q

What are the ACTH independent causes of Cushing’s syndrome?

A
  • latrogenic- steroid use (most common)
  • adrenal adenoma
165
Q

What are the signs and symptoms of Cushing’s?

A

moon face
central obesity
buffalo hump
acne
hypertension
striae
hirsutism
weight gain

166
Q

What is striae?

A

stretch marks

167
Q

What is hirsutism?

A

when women have excessive dark/ coarse hair in a male-like pattern (face/ chest/ back)

168
Q

What investigations are used for Cushing’s?

A
  1. random plasma cortisol- raised
  2. overnight dexamethasone suppression test- cortisol will not be suppressed in Cushing’s
  3. urinary free cortisol (24hr)
  4. plasma ACTH
169
Q

What is the treatment for Cushing’s?

A

treatment depends on the underlying cause:

  • latrogenic: stop medications if possible
  • Cushing’s disease: removal of pituitary adenoma (transsphenoidal surgery)
  • adrenal adenoma: adrenalectomy

cortisol inhibition drugs:
metyrapone
ketoconazole

170
Q

What is acromegaly?

A

release of excess growth hormone (GH) causing overgrowth of all systems

171
Q

What are the causes of acromegaly?

A
  • 99% of cases caused by pituitary adenoma
  • secondary to a malignancy that secretes ectopic GH (e.g. lung cancer)
172
Q

What are some complications of acromegaly?

A

erectile dysfunction
diabetes mellitus

173
Q

What are the signs and symptoms of acromegaly?

A

prominent forehead and brow
increased jaw size
large hands, nose, tongue, feet
bitemporal hemianopia
profuse sweating
lower pitch of voice
obstructive sleep apnoea

174
Q

What investigations are used for acromegaly?

A

1st line: insulin like growth factor 1 test - raised
gold standard: oral glucose tolerance test
other tests: random serum GH raised, MRI of pituitary fossa

175
Q

What is the treatment for acromegaly?

A

1st line- transsphenoidal resection surgery (if cause is adenoma)
2nd line- somatostatin analogue e.g. ocreotide
3rd line- GH receptor antagonist e.g. pegvisomant
4th line- dopamine agonist e.g. cabergoline

176
Q

What is transsphenoidal resection?

A

most common way to remove pituitary tumours

tumour removed via the sphenoid sinus, accessed through the nose

177
Q

What is a prolactinoma?

A

benign adenoma of pituitary gland producing excess prolactin

178
Q

What causes prolactinoma?

A

cause is unknown but there is a genetic association

179
Q

What is hyperprolactinaemia?

A

too much prolactin in the blood of men and women who aren’t pregnant

180
Q

What are some causes of hyperprolactinaemia other than prolactinoma?

A

non-functional pituitary tumour (compresses pituitary stalk hence no inhibition of prolactin release)

antidopaminergic drugs

181
Q

What are the 2 classifications of prolactinoma?

A

micro- tumour < 10mm diameter on MRI (most common, accounts for 90% of cases)

macro- tumour > 10mm diameter on MRI

182
Q

Why does prolactinoma cause galactorrhoea?

A

increased release of prolactin can cause galactorrhea by stimulating milk production from mammary gland as well as inhibiting FSH and LH

183
Q

What are the signs and symptoms of prolactinoma?

A

visual field defect
headache
menstrual irregularity
infertility
galactorrhea

184
Q

What investigations are used to diagnose prolactinoma?

A

prolactin levels
head CT

185
Q

What is the treatment for prolactinoma?

A
  • gold standard: transphenoidal resection surgery
  • 1st line: dopamine agonists: bromocriptine/ cabergoline
186
Q

Why are dopamine agonists used to treat prolactinoma?

A

dopamine has an inhibitory effect on prolactin

187
Q

What is Conn’s syndrome?

A

primary hyperaldosteronism due to an aldosterone producing adenoma

188
Q

Describe the pathophysiology of Conn’s syndrome

A

excess production of aldosterone independent of renin-angiotensin system:
- high sodium and water retention
- increased potassium excretion in kidneys
- low renin release

189
Q

What are the signs and symptoms of Conn’s syndrome?

A

hypertension
hypokalaemia
nocturia
polyuria
mood disturbance

190
Q

What investigations can confirm a diagnosis of Conn’s syndrome?

A
  • aldosterone-renin ratio blood test: increased
  • plasma potassium: reduced
  • U+E
191
Q

What is the treatment for Conn’s syndrome?

A
  • 1st line: spironolactone (pre-op controls BP and K+ levels)- if hyperplasia
  • gold standard: laparoscopic adrenalectomy- if adenoma

Aim is to lower BP, decrease aldosterone levels and resolve electrolyte imbalance

192
Q

What is Addison’s disease?

A

primary adrenal insufficiency

193
Q

Describe the pathophysiology of Addison’s disease

A

destruction of adrenal cortex leads to decreased production of glucocorticoid (cortisol) and mineralocorticoid (aldosterone)

194
Q

What are the causes of Addison’s disease?

A
  • autoimmune destruction (80% of cases in UK + developed countries)
  • TB (most common cause worldwide)
  • adrenal metastases
195
Q

What are the signs and symptoms of Addison’s disease?

A

tanned
lean
fatigue
pigmented palmar creases
postural hypotension
often diagnosed late

196
Q

What investigations can confirm a diagnosis of Addison’s disease?

A
  • 1st line:
    U+E confirms hyponatraemia, hypokalaemia
    Blood glucose confirms hypoglycaemia
  • Gold standard:
    Short SynACTHen test (ACTH stimulation test) presents with low cortisol, high ACTH
  • Plasma renin and aldosterone:
    high renin, low aldosterone
197
Q

What are some less commonly used test that can also confirm a diagnosis of Addison’s disease?

A
  • adrenal CT or MRI
  • 2l-hydroxylase adrenal autoantibodies- is positive in autoimmune diseases in more than 80% of cases
198
Q

What is the treatment for Addison’s disease?

A

replace steroids depending on signs and symptoms:
hydrocortisone- replaces cortisol
fludrocortisone- replaces aldosterone

treat underlying cause and warn against abruptly stopping steroids

199
Q

What does SIADH stand for?

A

syndrome of inappropriate ADH

200
Q

What is SIADH?

A

inappropriately large amounts of ADH secretion causing water to be reabsorbed in collecting duct

201
Q

What are the causes of SIADH?

A
  • post-operative from major surgery
  • infection (atypical pneumonia and lung abscess)
  • head injury
  • medications (thiazide diuretics)- most common cause
202
Q

What are the signs and symptoms of SIADH?

A

very non-specific
headache
nausea
fatigue
muscle cramps
confusion
severe hyponatraemia

203
Q

What investigations can confirm a diagnosis of SIADH?

A

DIAGNOSIS BY EXLCUSION
- U+E shows hyponatraemia
- high urine sodium
- high urine osmolality

Causes of hyponatraemia that need to be excluded:
- -ve short SynACTHen test- exclude adrenal insufficiency
- no diarrhoea, no vomiting
- no history of diuretic use
- no AKI/CKD

204
Q

How is SIADH managed?

A

treat underlying cause:
stop causative medicine
fluid restriction
tolvaptan (ADH receptor blocker)

205
Q

What is hyperkalaemia?

A

blood potassium level > 5.5mmol/L

206
Q

What are the causes of hyperkalaemia?

A

3 categories:

IMPAIRED EXCRETION:
- AKI/CKD
- drug affect (ACEi, NSAIDS, beta blockers)
- renal tubular acidosis
- addison’s disease (low aldosterone)

INCREASED INTAKE:
- IV K+ therapy
- increased dietary intake

SHIFT TO EXTRACELLULAR:
- metabolic acidosis
- rhabdomyolysis
- decreased insulin
- tumour lysis syndrome

207
Q

How does metabolic acidosis cause hyperkalaemia?

A

cells switch H+ for K+ to reduced acidosis

208
Q

Why does tumour lysis syndrome cause hyperkalaemia?

A

the intracellular contents (including potassium) are released

209
Q

What are the symptoms of hyperkalaemia?

A

fatigue
light-headedness
chest pain
palpitations

210
Q

What are the signs of hyperkalaemia?

A

arrhythmia (potential cardiac arrest)
reduced power and reflexes
flaccid paralysis
signs of underlying cause

211
Q

How will hyperkalaemia present on an ECG?

A
  • small/ absent p waves
  • prolonged PR interval (> 200ms)
  • wide QRS interval (> 120ms)
  • TALL TENTED T WAVES
212
Q

What investigations are used to confirm a diagnosis of hyperkalaemia?

A

ECG
bloods- FBC, U+E

213
Q

What is the treatment for hyperkalaemia?

A
  • ABC
  • cardiac monitoring
  • calcium gluconate- to protect myocardium
  • insulin and dextrose or nebuliser salbutamol - drives K+ intracellularly
  • treat underlying cause
214
Q

What is hypokalaemia?

A

blood potassium < 3.5mmol/L

215
Q

What are the causes of hypokalaemia?

A

3 categories:

INCREASED EXCRETION
- renal disease
- drug effect (thiazide, loop diuretics, laxatives)
- GI loss (D+V)
- Conn’s Syndrome

DECREASED INTAKE:
- dietary deficiency/ fasting
- liquorice abuse

SHIFT TO INTRACELLULAR:
- metabolic alkalosis
- drug effect (insulin, B2 agonists (SABAs and LABAs)

216
Q

What are the symptoms of hypokalaemia?

A

can be asymptomatic
fatigue + light headedness
weakness
cramps
palpitations
constipation

217
Q

What are the signs of hypokalaemia?

A

arrhythmia
hypotonia
hypereflexia
muscle paralysis
rhabdomyolysis

218
Q

How does hypokalaemia present on an ECG?

A
  • prolonged PR interval
  • ST depression
  • flat T waves
  • prominent U waves
219
Q

What investigations are used to confirm a diagnosis of hypokalaemia?

A

ECG
Bloods- FBC, U+E

220
Q

What are the two types of diabetes insipidus?

A

cranial
nephrogenic

221
Q

What are the symptoms of diabetes insipidus?

A

polyuria
polydipsia
dehydration

222
Q

Describe the pathophysiology of diabetes insipidus

A

caused by impaired water reabsorption from the kidneys

large volumes of dilute urine due to reduced ADH due to:

impaired secretion from posterior pituitary (cranial) OR impaired response of the kidney to ADH (nephrogenic)

223
Q

What are the causes of cranial diabetes insipidus?

A

can be idiopathic
congenital
tumour
trauma
infection

224
Q

What are the causes of nephrogenic diabetes insipidus?

A

inherited
metabolic (low potassium, high calcium)
drugs (lithium)
chronic renal disease

224
Q

What are the causes of nephrogenic diabetes insipidus?

A

inherited
metabolic (low potassium, high calcium)
drugs (lithium)
chronic renal disease

225
Q

How is diabetes insipidus diagnosed?

A

gold standard: 8hr water deprivation test to diagnose, then desmopressin test to establish if cranial or nephrogenic

other possible investigation: cranial MRI

226
Q

What is the treatment for diabetes insipidus?

A

treat underlying cause, mild cases can just undergo rehydration

cranial- desmopressin (synthetic ADH) to replace ADH
nephrogenic- if cause persists, give bendroflumethiazide

227
Q

What is desmopressin?

A

synthetic ADH

228
Q

What is hyperparathyroidism?

A

excessive secretion of parathyroid hormone (PTH)

229
Q

What are the categories of hyperparathyroidism?

A

PRIMARY- 1 parathyroid gland produced excessive PTH

SECONDARY- increased secretion of PTH to compensate hypocalcaemia

TERTIARY- autonomous secretion of PTH even after correction of calcium deficiency due to chronic kidney disease (CKD)

230
Q

What are the causes of primary hyperparathyroidism?

A

80% caused by adenoma
20% caused by hyperplasia of all glands

231
Q

What are the causes of secondary hyperparathyroidism?

A

chronic kidney disease (CKD)
low vitamin D

232
Q

What causes tertiary hyperparathyroidism?

A

develops from prolonged secondary hyperparathyroidism

233
Q

What are the signs and symptoms of hyperparathyroidism?

A

Bones, Stones, Moans, Groans, Hypercalcaemia

Bones- bone pain
Stones- renal calculi (kidney stones)
Moans- psychic moans (depression)
Groans- abdominal moans
Hypercalcaemia

234
Q

What investigations can be used to confirm a diagnosis of hyperparathyroidism?

A

PTH/ BONE PROFILE: high PTH, high calcium, low phosphates

PRIMARY- raised calcium
SECONDARY- low serum calcium, high PTH
TERTIARY- raised calcium + raised PTH

Can also do a DEXA scan X-ray which will show “salt and pepper” degradation of bone, and an ultrasound to look for kidney stones

235
Q

How is hyperparathyroidism managed?

A

“watchful waiting”

PRIMARY- surgical removal of adenoma, give bisphosphates
SECONDARY- calcium correction, treat underlying cause
TERTIARY- cinacalet (calcium mimetic), total/ part thyroidectomy

236
Q

What is hypoparathyroidism?

A

reduced PTH production
primary- due to gland failure
secondary- other causes

237
Q

What are the causes of hypoparathyroidism?

A

PRIMARY- failure of gland caused by:
autoimmune destruction
congenital (DiGeorge Syndrome)

SECONDARY-
surgical removal of thyroid gland
decreased magnesium (required for PTH secretion)

238
Q

What is DiGeorge Syndrome?

A

22q11 deletion

239
Q

What are the risk factors for hypoparathyroidism?

A

other autoimmune disorders

240
Q

Describe the pathophysiology of hypoparathyroidism

A

low PTH results in hypocalcaemia and hyperphosphateaemia which makes neurons more excitable

241
Q

What are the symptoms of hypoparathyroidism?

A

acronym: CATS go numb

Convulsions
Arrhythmias
Tetany
Spasm
Numbness

242
Q

What is tetany?

A

involuntary contraction of muscles

243
Q

What are the signs of hypoparathyroidism?

A
  • Chvostek’s sign- facial nerve tap induces spasm
  • Trousseau’s sign- BP cuff causes wrist flexion and fingers to pull together
244
Q

What investigations confirm a diagnosis of hypoparathyroidism?

A

Bloods- bone profiling
- decreased calcium
- increased or normal phosphate
- decreased PTH

ECG:
prolonged QT and ST segments

245
Q

What is the role of basal insulin in T1DM?

A

controls glucose levels between meals and at night
concentration can be adjusted as needed between 5-7mmol/L

246
Q

What is the role of bolus insulin?

A

manage glucose according to carbohydrate intake and pre-meal glucose

247
Q

Where is PTH secreted from?

A

chief cells in parathyroid gland

248
Q

How does PTH act on bone to increase serum calcium?

A

stimulates osteoclasts to release ionic calcium for reabsorption

249
Q

What hormone regulates the decrease in serum calcium?

A

calcitonin

250
Q

Where does calcitonin secretion occur?

A

c-cells in the thyroid, stimulated by increased serum calcium

251
Q

What is a normal level for serum calcium?

A

2.2 to 2.6 mmol/L

252
Q

What calcium levels would indicate hypocalcaemia?

A

mild-moderate: 1.9-2.2 mmol/L
severe: < 1.9 mmol/L

253
Q

What calcium levels would indicate hypocalcaemia?

A

mild-moderate: 1.9-2.2 mmol/L
severe: < 1.9 mmol/L

254
Q

Prolactinoma is a tumour of what cell type?

A

lactotroph

255
Q

Prolactinoma is a tumour of what cell type?

A

lactotroph

256
Q

What makes up the HPA axis?

A

hypothalamus
pituitary
adrenals

257
Q

What makes up the HPA axis?

A

hypothalamus
pituitary
adrenals

Phase 2a (18 decks)

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