Brainscape's Knowledge GenomeTM

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


See full index

UKMLA Prep > Endocrine and metabolic > Flashcards

Endocrine and metabolic Flashcards

Conditions and presentations

1
Q

What is the minimum HbA1c that would be diagnostic of type 2 diabetes mellitus?

A

6.5%
48 mmol/mol

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

Primary hyperparathyroidism

A

PTH (Elevated)
Ca2+ (Elevated)
Phosphate (Low)
Urine calcium : creatinine clearance ratio > 0.01

May be asymptomatic if mild
Recurrent abdominal pain (pancreatitis, renal colic)
Changes to emotional or cognitive state
Most cases due to solitary adenoma (80%), multifocal disease occurs in 10-15% and parathyroid carcinoma in 1% or less

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

Secondary hyperparathyroidism

A

PTH (Elevated)
Ca2+ (Low or normal)
Phosphate (Elevated)
Vitamin D levels (Low)
May have few symptoms
Eventually may develop bone disease, osteitis fibrosa cystica and soft tissue calcifications
Parathyroid gland hyperplasia occurs as a result of low calcium, almost always in a setting of chronic renal failure

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

Tertiary hyperparathyroidism

A

Ca2+ (Normal or high)
PTH (Elevated)
Phosphate levels (Decreased or Normal)
Vitamin D (Normal or decreased)
Alkaline phosphatase (Elevated) Metastatic calcification
Bone pain and / or fracture
Nephrolithiasis
Pancreatitis
Occurs as a result of ongoing hyperplasia of the parathyroid glands after correction of underlying renal disorder, hyperplasia of all 4 glands is usually the cause

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

Treatment of primary hyperparathyroidism

A

Indications for surgery
* Elevated serum Calcium > 1mg/dL above normal
* Hypercalciuria > 400mg/day
* Creatinine clearance < 30% compared with normal
———————————————————————————————-
Episode of life threatening hypercalcaemia
Nephrolithiasis
Age < 50 years
Neuromuscular symptoms
Reduction in bone mineral density of the femoral neck, lumbar spine, or distal radius of more than 2.5 standard deviations below peak bone mass (T score lower than -2.5)

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

Secondary hyperparathyroidism management

A

Usually managed with medical therapy.

Indications for surgery in secondary (renal) hyperparathyroidism:

  • Bone pain
  • Persistent pruritus
  • Soft tissue calcifications
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Tertiary hyperparathyroidism management

A
  • Allow 12 months to elapse following transplant as many cases will resolve
  • The presence of an autonomously functioning parathyroid gland may require surgery.
  • If the culprit gland can be identified then it should be excised.
  • Otherwise total parathyroidectomy and re-implantation of part of the gland may be required.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Primary amenorrhoea

A

Failure to establish menstruation by 15 in girls

Normal secondary sexual characteristics
such as breast development
Or
Age of 13 girls with no secondary sexual characteristics

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

Secondary amenorrhoea

A

Cessation of menstruation for 3-6 months in women with prev normal and regular menses

6-12 months in women with previous oligomenorrhoea

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

Primary causes of Amenorrhoea

A

gonadal dysgenesis (e.g. Turner’s syndrome) - the most common causes
testicular feminisation
congenital malformations of the genital tract
functional hypothalamic amenorrhoea (e.g. secondary to anorexia)
congenital adrenal hyperplasia
imperforate hymen

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

Secondary causes of amenorrhoea

A

hypothalamic amenorrhoea (e.g. secondary stress, excessive exercise)
polycystic ovarian syndrome (PCOS)
hyperprolactinaemia
premature ovarian failure
thyrotoxicosis (hypothyroidism)
Sheehan’s syndrome
Asherman’s syndrome (intrauterine adhesions)
Pregnancy

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

Investigations for amenorrhoea

A

exclude pregnancy with urinary or serum bHCG
full blood count, urea & electrolytes, coeliac screen, thyroid function tests
gonadotrophins
low levels indicate a hypothalamic cause where as raised levels suggest an ovarian problem (e.g. Premature ovarian failure)
raised if gonadal dysgenesis (e.g. Turner’s syndrome)
prolactin
androgen levels
raised levels may be seen in PCOS
oestradiol

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

Management of primary amenorrhoea

A

investigate and treat any underlying cause
with primary ovarian insufficiency due to gonadal dysgenesis (e.g. Turner’s syndrome) are likely to benefit from hormone replacement therapy (e.g. to prevent osteoporosis etC)

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

Secondary amenorrhoea

A

exclude pregnancy, lactation, and menopause (in women 40 years of age or older)
treat the underlying cause

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

What is ectopic pregnancy?

A

Implantation of a fertilized ovum outside the uterus results in an ectopic pregnancy

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

27 year old woman who presents to the emergency department with a history female with a history of 6-8 weeks amenorrhoea who presents with lower abdominal pain and later develops vaginal bleeding

A

Ectopic pregnancy

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

Ectopic pregnancy symptoms

A

lower abdominal pain
due to tubal spasm
typically the first symptom
pain is usually constant and may be unilateral.
vaginal bleeding
usually less than a normal period
may be dark brown in colour
history of recent amenorrhoea
typically 6-8 weeks from the start of last period
if longer (e.g. 10 wks) this suggest another causes e.g. inevitable abortion
peritoneal bleeding can cause shoulder tip pain and pain on defecation / urination
dizziness, fainting or syncope may be seen
symptoms of pregnancy such as breast tenderness may also be reported

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

Signs of ectopic pregnancy

A

abdominal tenderness
cervical excitation (also known as cervical motion tenderness)
adnexal mass: NICE advise NOT to examine for an adnexal mass due to an increased risk of rupturing the pregnancy. A pelvic examination to check for cervical excitation is however recommended

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

Pregnancy of unknown location investigation

A

case of pregnancy of unknown location, serum bHCG levels >1,500 points toward a diagnosis of an ectopic pregnancy

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

Osteomalacia

A

softening of the bones secondary to low vitamin D levels that in turn lead to decreased bone mineral content. If this occurs in growing children it is referred to as rickets, with the term osteomalacia preferred for adults.

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

Causes of osteomalacia

A

vitamin D deficiency
malabsorption
lack of sunlight
diet
chronic kidney disease
drug induced e.g. anticonvulsants
inherited: hypophosphatemic rickets (previously called vitamin D-resistant rickets)
liver disease: e.g. cirrhosis
coeliac disease

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

Features of Osteomalacia

A

bone pain
bone/muscle tenderness
fractures: especially femoral neck
proximal myopathy: may lead to a waddling gait

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

Investigations of osteomalacia

A

bloods
low vitamin D levels
low calcium, phosphate (in around 30%)
raised alkaline phosphatase (in 95-100% of patients)
x-ray
translucent bands (Looser’s zones or pseudofractures)

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

Treatment of osteomalacia

A
  • vitamin D supplementation
    A loading dose is often needed initially

calcium supplementation if dietary calcium is inadequate

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

Paget’s disease of the bone

A

primarily a disorder of osteoclasts, with excessive osteoclastic resorption followed by increased osteoblastic activity. Paget’s disease is common (UK prevalence 5%) but symptomatic in only 1 in 20 patients.

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

Which bones are commonly affected by Paget’s disease?

A

The skull, spine/pelvis, and long bones of the lower extremities are most commonly affected.

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

Predisposing factors for Paget’s’s disease

A

increasing age
male sex
northern latitude
family history

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

Clinical features of Paget’s disease?

A

only 5% of patients are symptomatic
the stereotypical presentation is an older male with bone pain and an isolated raised ALP
bone pain (e.g. pelvis, lumbar spine, femur)
classical, untreated features: bowing of tibia, bossing of skull

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

Investigations for Paget’s disease

A
  • bloods
  • other markers of bone turnover
  • X-rays
  • bone scintigraphy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Paget’s disease blood findings

A

raised alkaline phosphatase (ALP)
calcium and phosphate are typically normal. Hypercalcaemia may occasionally occur with prolonged immobilisation

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

Other markers of bone turnover in Paget’s disease

A

procollagen type I N-terminal propeptide (PINP)
serum C-telopeptide (CTx)
urinary N-telopeptide (NTx)
urinary hydroxyproline

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

X-rays Paget’s disease

A

osteolysis in early disease → mixed lytic/sclerotic lesions later
skull x-ray: thickened vault, osteoporosis circumscripta

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

Bone scintigraphy Paget’s disease

A

Increased uptake is seen focally at the sites of active bone lesion

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

Management of Paget’s disease

A

indications for treatment include
bone pain
skull or long bone deformity
fracture
periarticular Paget’s
bisphosphonate (either oral risedronate or IV zoledronate)
calcitonin is less commonly used now

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

Complications of bone disease

A

deafness (cranial nerve entrapment)
bone sarcoma (1% if affected for > 10 years)
fractures
skull thickening
high-output cardiac failure

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

Primary hyperparathyroidism

A

excess secretion of PTH resulting in hypercalcaemia. It is the most common cause of hypercalcaemia in outpatients and is often diagnosed following an incidental finding of an elevated serum calcium concentration.

In 85% of cases a parathyroid adenoma is responsible.

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

Causes of primary hyperparathyroidism

A

85%: solitary adenoma
10%: hyperplasia
4%: multiple adenoma
1%: carcinoma

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

Symptomatic features of primary hyperparathyroidism

A
  • 80% of patients may asymptomatic
    polydipsia, polyuria
    depression
    anorexia, nausea, constipation
    peptic ulceration
    pancreatitis
    bone pain/fracture
    renal stones
    hypertension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Primary hyperparathyroidism mnemonic

A

`Bones, groans, abdominal groans and psychic moans

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

Associations of primary hyperparathyroidism

A
  • hypertension
  • mutiple endocrine neoplasia: Men I and Men II
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Treatment of primary hyperparathyroidism

A

the definitive management is total parathyroidectomy
conservative management may be offered if the calcium level is less than 0.25 mmol/L above the upper limit of normal AND the patient is > 50 years AND there is no evidence of end-organ damage
patients not suitable for surgery may be treated with cinacalcet, a calcimimetic
a calcimimetic ‘mimics’ the action of calcium on tissues by allosteric activation of the calcium-sensing receptor

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

Investigations of primary hyperparathyroidism

A

bloods
raised calcium, low phosphate
PTH may be raised or (inappropriately, given the raised calcium) normal
technetium-MIBI subtraction scan
x-ray findings
pepperpot skull
osteitis fibrosa cystica

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

Gynaecomastia

A

abnormal amount of breast tissue in males and is usually caused by an increased oestrogen:androgen ratio. It is important to differentiate the causes of galactorrhoea (due to the actions of prolactin on breast tissue) from those of gynaecomastia

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

Causes of gynaecomastia

A

physiological: normal in puberty
syndromes with androgen deficiency: Kallman’s, Klinefelter’s
testicular failure: e.g. mumps
liver disease
testicular cancer e.g. seminoma secreting hCG
ectopic tumour secretion
hyperthyroidism
haemodialysis
drugs: see below

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

Drugs which cause gynaecomastia

A

spironolactone (most common drug cause)
cimetidine
digoxin
cannabis
finasteride
GnRH agonists e.g. goserelin, buserelin
oestrogens, anabolic steroids

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

Very rare drugs which cause gynaecomastia

A

tricyclics
isoniazid
calcium channel blockers
heroin
busulfan
methyldopa

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

Hypertension

A

a clinic reading persistently above >= 140/90 mmHg, or:
a 24 hour blood pressure average reading >= 135/85 mmHg

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

Primary hypertension

A

This is where there is no single disease causing the rise in blood pressure but rather a series of complex physiological changes which occur as we get older.

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

Secondary hypertension

A

caused by a wide variety of endocrine, renal and other causes.

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

Renal disease secondary hypertension

A

Glomerulonephritis
• Chronic pyelonephritis
• Adult polycystic kidney disease
• Renal artery stenosis

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

Endocrine disorders secondary hypertension

A

Primary hyperaldosteronism
• Phaeochromocytoma
• Cushing’s syndrome
• Liddle’s syndrome
• Congenital adrenal hyperplasia (11-beta hydroxylase deficiency)
• Acromegaly

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

Other causes of Secondary hypertension

A

Glucocorticoids
• NSAIDs
• Pregnancy
• Coarctation of the aorta
• Combined oral contraceptive pill

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

Signs and symptoms of hypertension

A

Typically asymptomatic
If above 200/120 patients may experience

headaches
visual disturbance
seizures

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

What else to check when suspecting hypertension

A

fundoscopy: to check for hypertensive retinopathy
urine dipstick: to check for renal disease, either as a cause or consequence of hypertension
ECG: to check for left ventricular hypertrophy or ischaemic heart disease

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

Investigation of 24hr blood pressure

A
  • 24 hour reasoning

-24 hour blood pressure monitoring is not available then home readings using an automated sphygmomanometer are useful.

urea and electrolytes: check for renal disease, either as a cause or consequence of hypertension
HbA1c: check for co-existing diabetes mellitus, another important risk factor for cardiovascular disease
lipids: check for hyperlipidaemia, again another important risk factor for cardiovascular disease
ECG
urine dipstick

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

Management of hypertension

A

drug therapy using antihypertensives
modification of other risk factors to reduce the overall risk of cardiovascular disease
monitoring the patient for the development of complications of hypertension

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

Angiotensin-converting enzyme (ACE) inhibitor

A

Inhibit the conversion angiotensin I to angiotensin II

Associated with cough, angioedema, hyperkalaemia

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

Calcium channel blockers

A

Block voltage-gated calcium channels relaxing vascular smooth muscle and force of myocardial contraction

Flushing
Ankle swelling
Headache

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

Thiazide type diuretics

A

Inhibit sodium absorption at the beginning of the distal convoluted tubule

Hyponatraemia
Hypokalaemia
Dehydration

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

Angiotensin II receptor blockers (A2RB)

A

Block effects of angiotensin II at the AT1 receptor

Hyperkalaemia

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

Stage 1 hypertension

A

Clinic BP >= 140/90 mmHg and subsequent ABPM daytime average or HBPM average BP >= 135/85 mmHg

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

Stage 2 hypertension

A

Clinic BP >= 160/100 mmHg and subsequent ABPM daytime average or HBPM average BP >= 150/95 mmHg

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

Severe hypertension

A

Clinic systolic BP >= 180 mmHg, or clinic diastolic BP >= 120 mmHg

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

the blood pressure is >= 180/120 mmHg:

A

admit for specialist assessment if:
signs of retinal haemorrhage or papilloedema (accelerated hypertension) or
life-threatening symptoms such as new-onset confusion, chest pain, signs of heart failure, or acute kidney injury
NICE also recommend referral if a phaeochromocytoma is suspected (labile or postural hypotension, headache, palpitations, pallor and diaphoresis)
if none of the above then arrange urgent investigations for end-organ damage (e.g. bloods, urine ACR, ECG)
if target organ damage is identified, consider starting antihypertensive drug treatment immediately, without waiting for the results of ABPM or HBPM.
if no target organ damage is identified, repeat clinic blood pressure measurement within 7 days

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

Amubulatory blood pressure

A

at least 2 measurements per hour during the person’s usual waking hours (for example, between 08:00 and 22:00)
use the average value of at least 14 measurements

If ABPM not tolerated, consider HBPM

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

HBPM

A

for each BP recording, two consecutive measurements need to be taken, at least 1 minute apart and with the person seated
BP should be recorded twice daily, ideally in the morning and evening
BP should be recorded for at least 4 days, ideally for 7 days
discard the measurements taken on the first day and use the average value of all the remaining measurements

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

ABPM/HBPM >= 135/85 mmHg (i.e. stage 1 hypertension)

A

treat if < 80 years of age AND any of the following apply; target organ damage, established cardiovascular disease, renal disease, diabetes or a 10-year cardiovascular risk equivalent to 10% or greater
in 2019, NICE made a further recommendation, suggesting that we should ‘consider antihypertensive drug treatment in addition to lifestyle advice for adults aged under 60 with stage 1 hypertension and an estimated 10-year risk below 10%. ‘. This seems to be due to evidence that QRISK may underestimate the lifetime probability of developing cardiovascular disease

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

ABPM/HBPM >= 150/95 mmHg (i.e. stage 2 hypertension)

A

OFFER DRUG REGARDLESS OF AGE

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

Mittelschmerz

A

translates to ‘middle pain’ and refers to abdominal pain associated with ovulation. This mid-cyclical pain is experienced by 20% of women and there are several theories as to why it occurs

occurs due to a leakage of follicular fluid containing prostaglandins at the time of ovulation, which causes the pain. Another explanation is that the growth of the follicle stretches the surface of the ovary, causing pain.

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

Presentation of Mittelschmerz

A

Sudden onset of pain in either iliac fossa which then manifests as a generalised pelvic pain.
Typically, the pain is not severe and varies in duration, lasting from minutes to hours.
It is self-limiting and resolves within 24 hours of onset.
Pain may switch side from month to month, depending on the site of ovulation

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

Investigation of Mittelschmerz

A

There is no specific test to confirm Mittelschmerz and it diagnosed clinically, after taking a full history and examination to exclude other conditions
No abnormal signs on abdominal or pelvic examination.

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

Management of Mittelschmerz

A

Mittelschmerz is not harmful and can be controlled with simple analgesia.

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

Dysmenorrhoea

A

excessive pain during the menstrual period. It is traditionally divided into primary and secondary dysmenorrhoea.

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

Primary dysmenorrhoea

A

underlying pelvic pathology. It affects up to 50% of menstruating women and usually appears within 1-2 years of the menarche. Excessive endometrial prostaglandin production is thought to be partially responsible.

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

Features of primary dysmenorrhea

A

pain typically starts just before or within a few hours of the period starting
suprapubic cramping pains which may radiate to the back or down the thigh

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

Management of primary dysmenorrhea

A

NSAIDs such as mefenamic acid and ibuprofen are effective in up to 80% of women. They work by inhibiting prostaglandin production
combined oral contraceptive pills are used second line

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

Secondary dysmenorrhea

A

develops many years after the menarche and is the result of an underlying pathology. In contrast to primary dysmenorrhoea the pain usually starts 3-4 days before the onset of the period.

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

Causes of secondary dysmenorrhea

A

endometriosis
adenomyosis
pelvic inflammatory disease
intrauterine devices- copper coil
fibroids

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

Heavy bleeding management

A

management has shifted towards what the woman considers to be excessive.
Treatment based on whether woman needs contraception

80
Q

Investigations of heavy bleeding

A

a full blood count should be performed in all women
NICE recommend arranging a routine transvaginal ultrasound scan if symptoms (for example, intermenstrual or postcoital bleeding, pelvic pain and/or pressure symptoms) suggest a structural or histological abnormality. Other indications include abnormal pelvic exam findings.

81
Q

Heavy bleeding does not require contraception

A

either mefenamic acid 500 mg tds (particularly if there is dysmenorrhoea as well) or tranexamic acid 1 g tds. Both are started on the first day of the period
if no improvement then try other drug whilst awaiting referral

82
Q

Require contraception heavy bleeding

A

intrauterine system (Mirena) should be considered first-line
combined oral contraceptive pill
long-acting progestogens

Norethisterone 5 mg tds can be used as a short-term option to rapidly stop heavy menstrual bleeding.

83
Q

PCOS

A

complex condition of ovarian dysfunction thought to affect between 5-20% of women of reproductive age.

The aetiology of PCOS is not fully understood. Both hyperinsulinaemia and high levels of luteinizing hormone are seen in PCOS and there appears to be some overlap with the metabolic syndrome.

84
Q

Features of PCOS

A

subfertility and infertility
menstrual disturbances: oligomenorrhoea and amenorrhoea
hirsutism, acne (due to hyperandrogenism)
obesity
acanthosis nigricans (due to insulin resistance)

85
Q

Investigations of PCOS

A

pelvic ultrasound: multiple cysts on the ovaries
NICE Clinical Knowledge Summaries recommend the following baseline investigatons: FSH, LH, prolactin, TSH, testosterone, sex hormone-binding globulin (SHBG) are useful investigations
raised LH:FSH ratio is a ‘classical’ feature but is no longer thought to be useful in diagnosis
prolactin may be normal or mildly elevated
testosterone may be normal or mildly elevated - however, if markedly raised consider other causes
SHBG is normal to low in women with PCOS
check for impaired glucose tolerance

86
Q

Diagnostic criteria of PCOS

A

a formal diagnosis should only be made after performing investigations to exclude other conditions
the Rotterdam criteria state that a diagnosis of PCOS can be made if 2 of the following 3 are present:
infrequent or no ovulation (usually manifested as infrequent or no menstruation)
clinical and/or biochemical signs of hyperandrogenism (such as hirsutism, acne, or elevated levels of total or free testosterone)
polycystic ovaries on ultrasound scan (defined as the presence of ≥ 12 follicles (measuring 2-9 mm in diameter) in one or both ovaries and/or increased ovarian volume > 10 cm³)

87
Q

General managment of PCOS

A

weight reduction if appropriate
if a women requires contraception then a combined oral contraceptive (COC) pill may help regulate her cycle and induce a monthly bleed (see below)

88
Q

Hirsutism and acne general management of PCOS

A

a COC pill may be used help manage hirsutism. Possible options include a third generation COC which has fewer androgenic effects or co-cyprindiol which has an anti-androgen action. Both of these types of COC may carry an increased risk of venous thromboembolism
if doesn’t respond to COC then topical eflornithine may be tried
spironolactone, flutamide and finasteride may be used under specialist supervision

89
Q

Infertility management of PCOS

A

weight reduction if appropriate
the management of infertility in patients with PCOS should be supervised by a specialist. There is an ongoing debate as to whether metformin, clomifene or a combination should be used to stimulate ovulation
a 2007 trial published in the New England Journal of Medicine suggested clomifene was the most effective treatment. There is a potential risk of multiple pregnancies with anti-oestrogen therapies such as clomifene. The RCOG published an opinion paper in 2008 and concluded that on current evidence metformin is not a first line treatment of choice in the management of PCOS
metformin is also used, either combined with clomifene or alone, particularly in patients who are obese
gonadotrophins

90
Q

Premenstrual syndrome

A

Premenstrual syndrome (PMS) describes the emotional and physical symptoms that women may experience in the luteal phase of the normal menstrual cycle.

PMS only occurs in the presence of ovulatory menstrual cycles - it doesn’t occur prior to puberty, during pregnancy or after the menopause.

91
Q

Emotional symptoms of PMS

A

anxiety
stress
fatigue
mood swings

92
Q

Physical symptoms of PMS

A
  • bloating
  • breast pain
93
Q

PMS mild symptom managment

A

apart from the usual advice on sleep, exercise, smoking and alcohol, specific advice includes regular, frequent (2-3 hourly), small, balanced meals rich in complex carbohydrates

94
Q

Moderate symptom managment of PMS

A

new-generation combined oral contraceptive pill (COCP)
examples include Yasminµ (drospirenone 3 mg and ethinylestradiol 0.030 mg)

95
Q

Several symptom managment of PMS

A

selective serotonin reuptake inhibitor (SSRI)
this may be taken continuously or just during the luteal phase (for example days 15-28 of the menstrual cycle, depending on its length)

96
Q

Addisons disease

A

Autoimmune destruction of the adrenal glands is the most common cause of primary hypoadrenalism in the UK, accounting for 80% of cases. This is termed Addison’s disease and results in reduced cortisol and aldosterone being produced

97
Q

Features of Addison’s disease

A

lethargy, weakness, anorexia, nausea & vomiting, weight loss, ‘salt-craving’
hyperpigmentation (especially palmar creases)

vitiligo
loss of pubic hair in women
hypotension
hypoglycaemia
hyponatraemia and hyperkalaemia may be seen
crisis: collapse, shock, pyrexia

98
Q

Hyperpigmentation in Addison’s disease

A

ACTH is derived from a larger precursor molecule called proopiomelanocortin (POMC). When POMC is cleaved to produce ACTH, other melanocyte-stimulating hormones (MSH) are also produced. These MSHs have the effect of stimulating melanocytes in the skin to produce more melanin, the pigment responsible for skin colour
primary Addison’s is associated with hyperpigmentation whereas secondary adrenal insufficiency is not

99
Q

Primary causes of hypoadrenalism

A

tuberculosis
metastases (e.g. bronchial carcinoma)
meningococcal septicaemia (Waterhouse-Friderichsen syndrome)
HIV
antiphospholipid syndrome

100
Q

Secondary causes of hypoadrenalism

A

pituitary disorders (e.g. tumours, irradiation, infiltration)

Exogenous glucocorticoid therapy

101
Q

Addison’s disease Associated electrolyte abnormalities are seen in around one-third of undiagnosed patients:

A

hyperkalaemia
hyponatraemia
hypoglycaemia
metabolic acidosis

102
Q

Definite investigation for Addison’s disease

A

ACTH stimulation test (short Synacthen test).

Plasma cortisol is measured before and 30 minutes after giving Synacthen 250ug IM. Adrenal autoantibodies such as anti-21-hydroxylase may also be demonstrated.

103
Q

If ACTH simulation is not available

A

> 500 nmol/l makes Addison’s very unlikely
< 100 nmol/l is definitely abnormal
100-500 nmol/l should prompt a ACTH stimulation test to be performed

104
Q

Management of Addison’s disease

A

glucocorticoid and mineralocorticoid replacement therapy.

hydrocortisone: usually given in 2 or 3 divided doses. Patients typically require 20-30 mg per day, with the majority given in the first half of the day
fludrocortisone

105
Q

Patient education on Addison’s disease

A

emphasise the importance of not missing glucocorticoid doses
consider MedicAlert bracelets and steroid cards
patients should be provided with hydrocortisone for injection with needles and syringes to treat an adrenal crisis
discuss how to adjust the glucocorticoid dose during an intercurrent illness (see below)

106
Q

Management of intercurrent illness in Addison’s disease

A

in simple terms the glucocorticoid dose should be doubled, with the fludrocortisone dose staying the same
the Addison’s Clinical Advisory Panel have produced guidelines detailing particular scenarios - please see the CKS link for more details

107
Q

Addisonian crisis causes

A

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

108
Q

Management 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

109
Q

DKA

A

complication of existing type 1 diabetes mellitus or be the first presentation, accounting for around 6% of cases. Rarely, under conditions of extreme stress, patients with type 2 diabetes mellitus may also develop DKA.

110
Q

Pathophysiology of DKA

A

DKA is caused by uncontrolled lipolysis (not proteolysis) which results in an excess of free fatty acids that are ultimately converted to ketone bodies

111
Q

Features of DKA

A

abdominal pain
polyuria, polydipsia, dehydration
Kussmaul respiration (deep hyperventilation)
Acetone-smelling breath (‘pear drops’ smell

112
Q

American Diabetes Association (2009) diagnostic criteria

A

glucose > 13.8 mmol/l
pH < 7.30
serum bicarbonate <18 mmol/l
anion gap > 10
ketonaemia

113
Q

Joint British Diabetes Societies (2013) diagnostic criteria

A

glucose > 11 mmol/l or known diabetes mellitus
pH < 7.3
bicarbonate < 15 mmol/l
ketones > 3 mmol/l or urine ketones ++ on dipstick

114
Q

Management of DKA

A

-fluid replacement
- insulin
-correction of electrolytes disturbance
-long-acting insulin should be continued, short-acting insulin should be stopped

115
Q

Fluid replacement of DKA

A

most patients with DKA are deplete around 5-8 litres
isotonic saline is used initially, even if the patient is severely acidotic

116
Q

Insulin management of DKA

A

an intravenous infusion should be started at 0.1 unit/kg/hour
once blood glucose is < 14 mmol/l an infusion of 10% dextrose should be started at 125 mls/hr in addition to the 0.9% sodium chloride regime

117
Q

Correction of DKA electrolyte disturbance

A

serum potassium is often high on admission despite total body potassium being low
this often falls quickly following treatment with insulin resulting in hypokalaemia
potassium may therefore need to be added to the replacement fluids
if the rate of potassium infusion is greater than 20 mmol/hour then cardiac monitoring may be required

118
Q

DKA resolution

A

pH >7.3 and
blood ketones < 0.6 mmol/L and
bicarbonate > 15.0mmol/L

Further points include

both the ketonaemia and acidosis should have been resolved within 24 hours. If this hasn’t happened the patient requires senior review from an endocrinologist
if the above criteria are met and the patient is eating and drinking switch to subcutaneous insulin
the patient should be reviewed by the diabetes specialist nurse prior to discharge

119
Q

Complications of DKA or the treatment

A

gastric stasis
thromboembolism
arrhythmias secondary to hyperkalaemia/iatrogenic hypokalaemia
iatrogenic due to incorrect fluid therapy: cerebral oedema hypokalaemia, hypoglycaemia
acute respiratory distress syndrome
acute kidney injury

120
Q

Cerebral oedema, children and DKA

A

children/young adults are particularly vulnerable to cerebral oedema following fluid resuscitation in DKA and often need 1:1 nursing to monitor neuro-observations, headache, irritability, visual disturbance, focal neurology etc. It usually occurs 4-12 hours following commencement of treatment but can present at any time. If there is any suspicion a CT head and senior review should be sought

121
Q

Features of head and neck cancer

A

neck lump
hoarseness
persistent sore throat
persistent mouth ulcer

122
Q

Laryngeal cancer

A

Consider a suspected cancer pathway referral (for an appointment within 2 weeks) for laryngeal cancer in people aged 45 and over with:
persistent unexplained hoarseness or
an unexplained lump in the neck

123
Q

Oral cancer

A

Consider a suspected cancer pathway referral (for an appointment within 2 weeks) for oral cancer in people with either:
unexplained ulceration in the oral cavity lasting for more than 3 weeks or
a persistent and unexplained lump in the neck.
Consider an urgent referral (for an appointment within 2 weeks) for assessment for possible oral cancer by a dentist in people who have either:
a lump on the lip or in the oral cavity or
a red or red and white patch in the oral cavity consistent with erythroplakia or erythroleukoplakia.

124
Q

Thyroid cancer

A

Consider a suspected cancer pathway referral (for an appointment within 2 weeks) for thyroid cancer in people with an unexplained thyroid lump.

125
Q

Reactive lymphadenopathy

A

By far the most common cause of neck swellings. There may be a history of local infection or a generalised viral illness

126
Q

Lymphoma

A

Rubbery, painless lymphadenopathy
The phenomenon of pain whilst drinking alcohol is very uncommon
There may be associated night sweats and splenomegaly

127
Q

Thyroid swelling

A

May be hypo-, eu- or hyperthyroid symptomatically
Moves upwards on swallowing

128
Q

Thyroglossal cyst

A

More common in patients < 20 years old
Usually midline, between the isthmus of the thyroid and the hyoid bone
Moves upwards with protrusion of the tongue
May be painful if infected

129
Q

Pharyngeal pouch

A

More common in older men
Represents a posteromedial herniation between thyropharyngeus and cricopharyngeus muscles
Usually not seen but if large then a midline lump in the neck that gurgles on palpation
Typical symptoms are dysphagia, regurgitation, aspiration and chronic cough

130
Q

Cystic hygroma

A

A congenital lymphatic lesion (lymphangioma) typically found in the neck, classically on the left side
Most are evident at birth, around 90% present before 2 years of age

131
Q

Branchial cyst

A

An oval, mobile cystic mass that develops between the sternocleidomastoid muscle and the pharynx
Develop due to failure of obliteration of the second branchial cleft in embryonic development
Usually present in early adulthood

132
Q

Cervical rib

A

More common in adult females
Around 10% develop thoracic outlet syndrome

133
Q

Carotid aneurysm

A

Pulsatile lateral neck mass which doesn’t move on swallowing

134
Q

Nipple discharge - physiological

A

During breast feeding

135
Q

Galactorrhoea

A

Commonest cause may be response to emotional events, drugs such as histamine receptor antagonists are also implicated

136
Q

Hyperprolactinaemia

A

Commonest type of pituitary tumour
Microadenomas <1cm in diameter
Macroadenomas >1cm in diameter
Pressure on optic chiasm may cause bitemporal hemianopia

137
Q

Mammary duct ectasia

A

Dilatation breast ducts.
Most common in menopausal women
Discharge typically thick and green in colour
Most common in smokers

138
Q

Carcinoma

A

Often blood stained
May be underlying mass or axillary lymphadenopathy

139
Q

Intraductal papilloma

A

Commoner in younger patients
May cause blood stained discharge
There is usually no palpable lump

140
Q

Assessment of nipple discharge

A

Examine breast and determine whether there is mass lesion present
All mass lesions should undergo Triple assessment.

141
Q

Elements of triple assessments

A
  • bi manual assessment
  • mammogram
  • needle biopsy
142
Q

reporting of investigations

A

1 No abnormality
2 Abnormality with benign features
3 Indeterminate probably benign
4 Indeterminate probably malignant
5 Malignant

143
Q

Management of non-malignant nipple discharge

A

Exclude endocrine disease
Nipple cytology unhelpful
Smoking cessation advice for duct ectasia
For duct ectasia with severe symptoms, total duct excision may be warranted.

144
Q

Cushing syndrome independent causes

A

iatrogenic: steroids
adrenal adenoma (5-10%)
adrenal carcinoma (rare)
Carney complex: syndrome including cardiac myxoma
micronodular adrenal dysplasia (very rare)

145
Q

Pseudo-Cushing’s

A

mimics Cushing’s
often due to alcohol excess or severe depression
causes false positive dexamethasone suppression test or 24 hr urinary free cortisol
insulin stress test may be used to differentiate

146
Q

ACTH dependent causes of Cushing

A

Cushing’s disease (80%): pituitary tumour secreting ACTH producing adrenal hyperplasia
ectopic ACTH production (5-10%): e.g. small cell lung cancer is the most common causes

147
Q

Epidemiology of Cushing

A

exogenous causes of Cushing’s syndrome (e.g. glucocorticoid therapy) are far more common than endogenous ones.

148
Q

Cushing ABG findings

A

hypokalaemic metabolic alkalosis may be seen, along with impaired glucose tolerance.

Ectopic ACTH secretion (e.g. secondary to small cell lung cancer) is characteristically associated with very low potassium levels.

149
Q

What three tests are used to confirm Cushing’s

A

overnight (low-dose) dexamethasone suppression test

24 hr urinary free cortisol

Bedtime salivary cortisol

150
Q

overnight (low-dose) dexamethasone suppression test

A

this is the most sensitive test and is now used first-line to test for Cushing’s syndrome
patients with Cushing’s syndrome do not have their morning cortisol spike suppressed

151
Q

24 hr urinary free cortisol

A

two measurements are required

152
Q

Bedtime salivary cortisol

A

two measurements are required

153
Q

Cortisol ACTH
Not suppressed Suppressed

A

Cushing’s syndrome due to other causes (e.g. adrenal adenomas)

154
Q

Cortisol suppresses and ACTH not suppressed

A

Cushing’s disease (i.e. pituitary adenoma → ACTH secretion)

155
Q

Cortisol and ACTH not suppressed

A

Ectopic ACTH syndrome

156
Q

Other tests for cushings

A

CRH stimulation
if pituitary source then cortisol rises
if ectopic/adrenal then no change in cortisol

Petrosal sinus sampling of ACTH may be needed to differentiate between pituitary and ectopic ACTH secretion.

An insulin stress test is used to differentiate between true Cushing’s and pseudo-Cushing’s.

157
Q

Managment of Cushing’s syndrome

A

Primary treatment is surgical removal of the underlying cause (e.g., adrenal tumor, pituitary adenoma).
If surgery isn’t feasible or unsuccessful, medical therapy may include adrenal enzyme inhibitors (e.g., ketoconazole, metyrapone), cortisol receptor blockers (e.g., mifepristone), or pituitary-directed drugs (e.g., pasireotide).
Close monitoring of symptoms, cortisol levels, and potential complications (e.g., osteoporosis, hypertension) is crucial.
Lifestyle modifications such as dietary changes and exercise may be recommended to manage weight gain and other associated symptoms

158
Q

Complications of Cushing’s syndrome”

A

Hypertension
Osteoporosis
Diabetes mellitus
Muscle weakness
Skin changes
Mood disturbances
Menstrual irregularities and infertility
CVD
Increased susceptibility to infection

159
Q

Acromegaly

A
  • Rare conditon which is caused by growth hormone-secreting pituitary adenoma
160
Q

Growth hormone releasing hormone (GHRH) independent acromegaly

A
  • ** Pituitary adenoma: **
  • Primary pituitary hyperplasia:
161
Q

Growth hormone releasing hormone (GHRH) dependent acromegaly

A
  • Hypothalamic source
  • Ectopic GHRH release
162
Q

Pathophysiology of acromegaly

A

Excess growth hormone (GH) results in excess production of insulin-like growth factor 1 (IGF-1)

163
Q

gigantism vs acromegaly

A
  • gigantism occurs before epiphyseal plate closure, leading to excessive linear growth.
  • Acromegaly occurs after plate closure, causing enlargement of bones and soft tissues.
164
Q

Signs and symptoms of acromegaly

A
165
Q

Investigations of acromegaly

A
  1. Bedside tests
    * urine dip
    * ecg
    * fundoscopy +perimertry

2.** Bloods**
* IGF1
* oral glucose tolerance test
* anterior pituitary profile

3.** Radiology**
* CXR (cardiomegaly)
* MRI Pituitary (adenoma)
* If considering an ectopic source, can do CTCAP

  1. Specialty tests
    * Sleep studies
    * colonoscopy
166
Q

anterior pituitary profile- what tests

A
  • TFT
  • LH
  • FSH
  • Prolactin
  • Oestrogen
  • Testosterone
  • Cortisol
  • HBA1c
167
Q

Acromegaly managment

A

1.Surgery
Transphenoidal (first line)/transfrontal resection of the pituitary +/-radiotherapy

  1. **Drug managment **
    * octreotide, lanreorid
    * Growth hormone antagonists (pegvisomant)
    * Dopamine agonists (bromocriptine, cabergoline)
  2. follow up
    * monitor for bowel changes
    * blood tests to make sure no reoccurance
168
Q

Complications of acromegaly

A
169
Q

Clinical features of Addison’s disease

A
  • Hypotension
  • Fatigue and weakness
  • Gastrointestinal symptoms
  • Syncope
  • Skin pigmentation due to increased ACTH which stimulates production of alpha melanocyte stimulating hormone (MSH).
170
Q

Investigations for Addison’s disease

A
  • U+E and serum cortisol
  • ACTH
  • Renin
  • aldosterone
  • Testing for adrenal auto-antibodies
  • Chest X-ray
  • CT scan of the adrenal glands
  • MRI of the brain
171
Q

Blood gas findings in Addison’s

A
  • hyperkalaemic
  • hyponatraemic,
  • hypoglycaemic metabolic acidosis
172
Q

gold standard investigation to confirm the addison’s.

A

ACTH (Short Synacthen) test

173
Q

Addison’s sick day rules?

A

Doubling the regular steroid medication dose during any intercurrent illness

174
Q

Managment of Addison’s crisis

A
  • Aggressive fluid resuscitation
  • Administration of intravenous/IM (if no access) steroids STAT
  • Glucose administration if hypoglycaemia is present
175
Q

What is Addison’s crisis

A

life-threatening condition that occurs when the body experiences a severe deficiency in cortisol

176
Q

Signs and symptoms of Addison’s crisis

A

Sudden and severe weakness
Fatigue
Nausea and vomiting
Abdominal pain
Low blood pressure
Dehydration
Confusion or loss of consciousness

177
Q

Causes of Addison’s crisis

A

Inadequate cortisol production due to adrenal gland dysfunction
Stressful events such as infections, trauma, or surgery
Sudden withdrawal of corticosteroid medications
Adrenal hemorrhage or infarction

178
Q

Managment of Addison’s crisis

A

Immediate administration of intravenous hydrocortisone
Fluid replacement to address dehydration and low blood pressure
Correction of electrolyte imbalances, particularly sodium and potassium levels
Management of any underlying causes or triggers

179
Q

Addison’s crisis prevention

A

Proper adherence to corticosteroid replacement therapy in individuals with Addison’s disease
Awareness of stressors that may precipitate a crisis and proactive management
Carrying medical identification indicating adrenal insufficiency status
Education of family members and caregivers regarding signs and management of Addison’s crisis

180
Q

Complications of Addison’s disease

A
  • Addisonian crisis (life-threatening adrenal crisis)
  • Severe electrolyte imbalances
  • Cardiovascular collapse
  • Hypoglycemia
  • Side effects of long term corticosteroid use e.g. osteoporosis
181
Q

Diabetes insipidus

A

condition characterized by the reduced production or response to antidiuretic hormone (ADH), resulting in excessive urination and thirst.

182
Q

Types of DI

A
  • Cranial
  • Nephrogenic
183
Q

cranial DI

A
  • Head trauma
  • Inflammatory conditions (e.g., sarcoidosis)
  • Cranial infections such as meningitis
  • Vascular conditions such as sickle cell disease
  • Rare genetic causes
184
Q

Nephrogenic DI

A
  • Drugs (e.g., lithium)
  • Metabolic disturbances (e.g., hypercalcaemia, hypokalaemia, hyperglycaemia)
  • Chronic renal disease
  • Rare genetic causes (e.g., Wolfram’s syndrome)
185
Q

Drugs which cause DI

A
  • Lithium:
  • Tetracyclines:
  • Antifungals: Medications like amphotericin B.
  • Antivirals:
  • Nonsteroidal Anti-inflammatory Drugs (NSAIDs): Such as ibuprofen.
186
Q

Features of DI

A

Large volumes of dilute urine (>3 litres in 24 hours and a urine osmolality of <300 mOsm/kg)
Nocturia
Excessive thirst
——————————————
In childten
Failure to thrive
Enuresis

187
Q
A
188
Q

DI investigations

A
  • Urea and electrolytes (sodium may be raised)
  • Blood glucose (to rule out diabetes mellitus)
  • Urine dip
  • Paired serum and urine osmolality measurements
189
Q

Serum osmolality DI

A

serum osmolality is raised** (>295 mOsm/kg) with inappropriately dilute urine (urine osmolality < 300 mOsm/kg).**

If the diagnosis remains uncertain then water deprivation

190
Q

Cranial DI managment

A
  • Cranial diabetes insipidus can be managed with desmopressin
  • Sodium levels should be monitored routinely due to the risk of hyponatraemia.
191
Q

Nephrogenic Diabetes Insipidus

A
  • Correcting any underlying metabolic abnormalities
  • discontinuing any offending drugs.
  • High dose desmopressin (meh)
  • Thiazide diuretic
  • non-steroidal anti-inflammatory drug to reduce urine volume.
192
Q

Amiodarone- induced thyroxicosis

A
  • Recognized adverse effect of the anti-arrhythmic agent.
  • Amiodarone is rich in iodine,
193
Q

Types of amiodarone induced thyrotoxicosis

A
  • AIT type 1 - direct toxic effect of amiodarone on the thyroid gland causing thyroiditis,
  • AIT type 2-amiodarone triggers underlying thyroid autoimmunity.
194
Q

AIT side effects

A

Weight loss
Tremors
Palpitations
Nervousness
Fatigue

195
Q
A
196
Q

hyperprolactinemia symptoms in women

A
  • galactorrhea
  • menstruation issues

UKMLA Prep (30 decks)

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