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Phase 2a > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What are the 4 hormones involved in appetite regulation?

What do each of them do and detect?

A

INCREASE SATIETY AND REDUCE APPETITE
Leptin - detects lipids
Insulin - detects carbohydrates

REDUCE SATIETY AND INCREASES APPETITE
Ghrelin and GLP-1 (glucagon-like peptide 1)

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2
Q

Difference between Cushing’s syndrome and Cushing’s disease

A

Cushing’s syndrome: general term for chronic excessive and inappropriate elevated levels of circulating CORTISOL

Cushing’s disease: excessive cortisol resulting from inappropriate ACTH secretion due to pituitary tumour

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3
Q 
CUSHING'S BACKGROUND
What releases CRH? Full name?
What releases ACTH? Full name?
What releases cortisol?
Proportion in blood? Bound to?
Effects of cortisol (6)
A

Hypothalamus releases corticotrophin releasing hormone.

Pituitary gland releases adenocorticotrophic hormone.

Zona fasiculata releases cortisol.

95% cortisol binding globulin, 5% free

Increased gluconeogenesis, proteolysis, lipolysis. Increased BP. Anti-inflammatory. Mood and memory.

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4
Q

CUSHING’S SIGNS AND SYMPTOMS
Big 3?
Others?

A

MOON FACE, OBESITY, BUFFALO HUMP

Mood changes, infection?, thin skin, bruises, osteoporosis, purple striae, acne, increased BP

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5
Q

CUSHING’S DIFFERENTIAL DIAGNOSIS?

A

Pseudo-Cushing’s syndrome

Caused by alcohol excess - resolves with abstinence

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6
Q

CUSHING’S DIAGNOSIS?
Initial?
First line?
2nd line?

A

Initial - urine, blood, saliva cortisol
First line - dexamethasone suppression test
(overnight or 48hr)
Second line - ACTH test and dexamethasone injected
ACTH high - pituitary or ectopic
ACTH low - adrenal tumours
CT and MRIs to confirm

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7
Q

CUSHING’S CAUSES?

A

Exogenous - oral steroids (most common)
Endogenous -
ACTH dependent: pituitary or ectopic
ACTH independent: adrenal tumour

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8
Q

CUSHING’S TREATMENT?

A

Stops steroids
Surgery on tumours
Medications: inhibit cortisol synthesis, eg METYRAPONE, KETOCONAZOLE, FLUCONAZOLE

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9
Q

ACROMEGALY vs GIGANTISM?

A

Acromegaly - hormone disorder in adults as a result of excess growth hormone
Gigantism - excess growth hormone in childhood, leading to increased height

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10
Q

ACROMEGALY BACKGROUND
Feedback mechanisms on GH?
Two groupings for GH effects? Examples?

A

GHRH from hypothalamus stimulates
Somatostatin from muscle, liver, bones inhibits

Direct: 
increased metabolism and growth
increased bone thickness and muscle
growth
increased insulin resistance
increased glucose in blood

Indirect: via IGF-1
increased metabolism, increased cell division and differentiation, prevents cell death

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11
Q 
ACROMEGALY EPIDEMIOLOGY AND RISK FACTORS
How common?
Male vs Female?
Age?
Specific risk factor
A

Rare - 3 per million in the UK
Male = Female
Middle age
MEN-1 (multiple endocrine neoplasia)

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12
Q

ACROMEGALY CAUSES
Main?
3 others?

A

99% of cases: functional pituitary adenoma
also:
ectopic, hypothalamic tumour, MEN-1

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13
Q

ACROMEGALY SIGNS AND SYMPTOMS
List as many as possible.
Note on diagnosis?

A

Often takes years to diagnose

Headaches
increased size of extremities
sweating
snoring
decreased libido
amenorrhea
skin darkens
wide nose
deep voice
macroglossia
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14
Q

ACROMEGALY COMPLICATIONS

5 examples

A 
Impaired glucose tolerance (40%)
Leading to diabetes mellitus (15%)
Carpal tunnel syndrome
HTN, cardiac problems
Colon cancer
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15
Q

ACROMEGALY DIAGNOSIS

3 steps

A

Test for increased IGF-1 (diagnostic) and GH (non-diagnostic)
Oral glucose tolerance test (OGTT) - glucose should suppress GH
MRI for pituitary adenoma

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16
Q

ACROMEGALY TREATMENT
1st line?
2nd line?
3rd line?

A

1: Trans-sphenoidal surgery (+radiotherapy?)
2: Somatostatin analogues, eg octreotide or lanreotide
3: GH antagonist (pregvisomant)

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17
Q

ADRENAL INSUFFICIENCY CAUSES

2 categories? Examples?

A

Primary (ADDISON’S DISEASE)
autoimmune (80%)
TB, metastatic carcinoma, lymphoma, CMV in HIV, adrenal haemorrhage

Secondary
long term steroid use
hypothalamic-pituitary disease (ACTH)

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18
Q

ADRENAL INSUFFICIENCY EPIDEMIOLOGY
How common?
Can it be fatal? Expand on this

A

Rare - 0.3 per 100,000
Can be fatal - ADDISONIAN CRISIS
untreated w/ bad destruction, leads to dehydration, low BP, tachycardia: possibly death

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19
Q

ADRENAL INSUFFICIENCY SIGNS AND SYMPTOMS?

Split up into 3 categories

A
  1. Due to lack of aldosterone
    hyperkalaemia, hyponatraemia, hypovolemia, metabolic acidosis, craving salts, NAUSEA, fatigue
  2. Due to lack of cortisol
    glucose down, weakness, tiredness, BRONZE PIGMENTATION
  3. Due to lack of androgens
    women only: decreased libido and changes/decreases in body hair
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20
Q

ADRENAL INSUFFICIENCY DIAGNOSIS & TREATMENT
First line?
Second line?

A

1st Blood tests:
sodium, potassium, hormones, etc
2nd ACTH stimulation test:
synthetic ACTH given, measure the cortisol and aldosterone, should increase if healthy

Treatment: Replace hormones
HYDROCORTISONE/PREDNISOLONE (gluco-)
FLUDROCORTISONE (mineral-)

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21
Q

HYPERALDOSTERONISM BACKGROUND
What are the actions of aldosterone? On what cells?
Use these to show signs of hyperaldosteronism.

A 
Principle cell (Na+ and H20 in, K+ out)
Hypernatermia, Hypervolemia, Hypokalaemia

Alpha Intercalated Cell (H+ excretion)
Metabolic alkalosis

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22
Q

HYPERALDOSTERONISM EPIDEMIOLOGY AND RISK FACTORS
What is HYPERALDOSTERONISM a rare cause of? How much?
When to check for HYPERALDOSTERONISM?

A

Rare cause of HTN (less than 1%)

Check for patients with HTN under 35 with no family history

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23
Q

HYPERALDOSTERONISM CAUSES
2 categories?
2 (w/ numbers) x 2

A

Primary (pathology with adrenal gland)

  • adrenal adenoma (CONN’S SYNDROME) (2/3)
  • idiopathic bilateral hyperplasia (1/3)

Secondary (pathology elsewhere, increased Renin)

  • chronic low BP (heart failure)
  • reduced renal perfusion
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24
Q

HYPERALDOSTERONISM CLINICAL FEATURES?
Often?
5.

A

OFTEN ASYMPTOMATIC
Hypertension, Muscle weakness and paraesthesiae
Polydipsia, polyuria

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25
Q

HYPERALDOSTERONISM DIAGNOSIS
1st tests
2nd tests

A

Blood tests: U and Es, Aldo, Renin (ARR)
ECG: (hypokalaemia)

24hr aldosterone test (confirmatory)
Adrenal CT scan

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26
Q

HYPERALDOSTERONISM TREATMENT
Main principle:
3 leads from this principle.
Specific medication?

A

= Treat the cause

  • Conn’s (surgery)
  • Bilateral Hyperplasia (medication - oral spironolactone, potassium sparing diuretic)
  • Heart Failure (normal treatment)
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27
Q

How are pituitary tumours categorised?

3 ways with examples

A

Size
- microadenoma <1cm, macroadenoma >1cm

Functional (less common - prolactinioma, Cushing’s disease, main cause of Acromegaly)
Non-functional (more common)

Histology
Chromophobe
Acidophil - somatotrophs, lactrotrophs
Basophil - corticotroph, thyrotrophs

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28
Q

3 key signs of a large pituitary tumour

A

Bilateral temporal hemianopia - starts at top
Palsy of cranial nerves III, IV, VI (eye movement)
CSF rhinorrhoea

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29
Q

What is a pituitary apoplexy?

When do it occur?

A

A rapid pituitary enlargement due to bleeding into the tumour
Very serious - needs urgent treatment

Can occur as a complication of a pituitary tumour

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30
Q

What is a prolactinoma?
Symptoms? - M vs W
How is it treated? Main example and other

A

Functional adenoma of lactotrophs that secrete prolactin.

W: Amenorrhea and galactorrhea
M: Low libido and gynecomastia

Treated with BROMOCRIPTINE (main) or CABERGOLINE (dopamine agonists)
Treated with surgery if macroadenoma

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31
Q

What is a craniopharngioma?
Mostly occurs in?
Symptoms?

A

Tumour orgininates from Rathke’s pouch

Most commonly occurs in children - causes hypopituitarism symptoms and pituitary gland tumour symptoms

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32
Q 
What is a neuroblastoma?
Who does it occur in?
Symptoms?
3 types?
Dx and Management?
A

Tumour of neuroblasts - don’t differentiate properly when forming the adrenal medulla

Usually in infants (less than 5 years old)

Fever, weight loss, sweating, BRUISING AROUND EYES

Differentiated, undifferentiated, poorly differentiated.

CT scan, adrenaline and noradrenaline metabolites (HMA and VMA)
Surgery, chemotherapy, stem cell or bone marrow transplant

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33
Q

What is a pheochromocytoma?
What is the base cell?
Symptoms?
Dx and management?

A

Rare adrenal gland tumour in the medulla - characterised by the darkening of cells

Chromaffin cells

PHEochromocytoma:
palpitations, headaches, episodic sweating

Test for catecholamines in blood
Surgery

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34
Q

Causes for thyroid nodules?

A 
Multinodular goitre
Benign follicular adenoma
Thyroid cysts
(95% - benign)
Thyroid cancers
(5%)
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35
Q

Types of thyroid cancers?
Which are the most common?
Which are the most aggressive?
Who do they normally occur in?

A

DIFFERENTIATED:
papillary (70%) - from follicular cells, young
follicular (20%) - from follicular cells, middle age
medullary (5%) - from calcitonin C cells
Anaplastic - (>5%) from follicular, aggressive, poor prognosis

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36
Q

Clinical presentation in thyroid tumours

A

Solitary, painless nodule (hard and immovable)

Later: dysphagia or hoarseness of voice from tumour, goitre?

37
Q

How to diagnose thyroid tumours? 4 possible tests

A

Fine needle aspiration
Blood tests - TSH, T4, T3, calcitonin
Radioiodine scan (normally cold)
Thyroid ultrascan

38
Q

How to treat thyroid cancers?

A

Thyroidectomy (partial or full)
Thyroid Hormone Replacement (TSH is a growth factor to cancer: will keep it down)
Chemotherapy

39
Q

What is goitre? Two types and causes of these types?

A

= enlarged thyroid gland

Diffuse = physiological, Grave's, Hasimoto's
Nodular = multinodular, adenoma, cyst, carcinoma
40
Q

Prevalence of hypothyroidism vs hyperthyroidism

A 
HYPER = 2,5%
HYPO = 5%
41
Q

Summary of Grave’s disease pathophysiology?

Antibody?

A

Autoimmune disease inducing excess production of thyroid hormone
Main: TSH Receptor antibody (TSHR-Ab)

42
Q 
GRAVE'S DISEASE EPIDEMIOLOGY AND RISK FACTORS
Fraction cause of hyperthyroid?
Females vs Males?
Age?
Other risk factors?
A

2/3 cause of HYPERTHYROID
Females&raquo_space; Male (9:1)
40-60 years old
Genetics, stress, smoking, other AI diseases

43
Q

GRAVE’S DIAGNOSTIC TRIAD?

A

Hyperthyroidism: weight loss, despite appetite, goitre, heat intolerance, increased heart rate, sweating, anxiety, thin hair

Grave’s opthalmopathy:
inflammation and sweating of eyes, lid lag, exopthalmos

Grave’s dermopathy:
Pretibial myxoedema - waxy, orange, swelling on anterior of feet

44
Q

MAJOR COMPLICATION OF HYPERTHYROIDISM?
Name?
Symptoms?

A

Thyroid storm - needs immediate treatment
Heat intolerance into HIGH FEVER
Tachycardia into CARDIAC ARRHYTHMIA

45
Q

DIAGNOSTIC TESTS FOR THYROID DISORDERS?

A

Measure TSH, T3, T4
Antibodies (TPO-Ab, TSHR-Ab, Tg-Ab)
Radioiodine scans
FBC for anaemia?

46
Q

4 POSSIBLE MANAGEMENT STRATEGIES FOR GRAVE’S?

A

Beta-blockers (propanolol)
Anti-thyroid drugs (carbimazole)
Radio-iodine therapy
Thyroidectomy

47
Q

Causes of hyperthyroidism? As many as possible

A

Grave’s (main), toxic multinodular goitre, functional thyroid adenoma, thyroiditis, Jod-Basedow (iodine intake), drugs (amiodarone), neonatal, ectopic

TSH pituitary tumour

48
Q

Hyperthyroidism symptoms? As many as possible

A

Weight loss, heat intolerance, fast HR, sweating, anxiety, insomnia, tremor, irritance, diarrhoea, menstrual changes, thin hair, Grave’s specific pathologies

49
Q

What is Hashimoto’s thyroiditis?

Antigens?

A

Thyroid gland is attacked by immune system?
TPO-Ab (thyroid peroxidase antibody)
TgAb (thyroglobulin antibody)

50
Q

HASHIMOTO’S THYROIDITIS: symptoms, and risk factors, management?

A

Early: often asymptomatic
Later: intial goitre, later shrinkage, goitre

Women&raquo_space; Men (7:1), other AI diseases, family history

Levothyroxine treatment (thyroid replacement)

51
Q

Causes of hypothyroidism? As many as possible

A

Iodine deficiency, Hashimoto’s thyroiditis, atrophy, surgery, drug-induced (anti-thyroid, amiodarone)

Tumour of anterior pituitary, hypothalamic damage

52
Q

Hypothyroidism symptoms? As many as possible

BRADYCARDIC (signs)

A 
Weight gain, cold sensitivity, decreased HR, mental slowness, tiredness, lethargy, low mood, constipation
B
Reflexes
Ataxia
Dry skin
Yawning/Tiredness
Cold sensitivity
Ascites
Round face/weight gain
Depression
Immobile
Cystic fibrosis
53
Q

MAJOR COMPLICATION OF HYPOTHYROIDISM?

Symptoms?

A

MYXOEDEMA COMA (severe)
Exaggerated hypothyroidism symptoms:
mental slowness, hypothermia, confusion

54
Q 
siADH BACKGROUND
Other name for ADH?
What receptor does ADH bind to?
What does it cause in the kidney?
What triggers release?
Biggest cause of what?
A

Vasopessin
V2 receptor
Causes aquaporin 2 channels to merge with membrane, causing increased water retention in blood
Triggered by high osmolarity or decrease in blood volume
25% cause of hyponatraemia

55
Q

siADH AETIOLOGY

List some causes? Categories

A

Ectopic tumours - release ADH

CNS - strokes, meningitis, trauma

Pulmonary lesions

Hypothyroidism, alcohol withdrawel, drugs

56
Q

siADH SIGNS AND SYMPTOMS
Mild and Severe: list as many as possible
Signs

A

Mild: nausea, vomiting, lethargy
Severe: muscle cramps, weakness, confusion, ataxia, tremors

Signs: decreased level of consciousness, cognitive impairment, seizures, etc

57
Q 
siADH DIAGNOSIS
What would serum and urine sodium be?
Hence, plasma and urine osmolality?
Which -volaemia?
Why test with saline?
A

Serum sodium low
Urine sodium high
Plasma osmolality low
Urine osmolality high

Normally, euvolaemic

Test with saline - may just be sodium deficient, especially elderly

58
Q

siADH management
Principle?
Diet change?
Two drugs?

A

Treat underlying cause
Restrict fluid intake and increase sodium intake
ORAL DEMECLOCYCLINE - induces nephrogenic DI
ORAL TOLVAPTAN - V2 blocker, very expesnive

59
Q

Diabetes Insipidus can be defined as…

Number?

A

Large volume of dilute urine produced, due to impaired water reabsorption
>3L per day

60
Q

Two categorical causes of DI with examples?

A

Cranial DI: decreased ADH
idiopathic, congenital, hypothalamic disease, pituitary tumour, sarcoidosis

Nephrogenic DI: can’t bind or kidney damage
CKD, metabolic disorders, gene mutations, drugs

61
Q

Clinical presentation of DI?

Differential diagnosis?

A

Polyuria, nocturia, polydipsia, general dehydration
NO GLYCOSURIA

Rules out main ddx: diabetes mellitus
Also: hypokalaemia and hypercalcaemia

62
Q

Two diagnostic tests for DI?

A

Fluid Deprivation Test:
Urine osmolality will stay low

IM DESMOPRESSIN (ADH analogue)
Cranial DI: will be fixed
Nephrogenic DI: won’t be fixed

63
Q

How to treat cranial DI vs nephrogenic DI?

A

Cranial: give desmopressin, find cause, stop it

Nephrogenic: find cause and stop it, high dose desmopressin, diet control, NSAIDs & Bendroflumethiazide (both inhibit ADH)

64
Q

PARATHYROID BACKGROUND
What cells produce parathyroid hormone (PTH)?
What are the 4 actions of PTH?

A

Chief cells

  • Calcium absorption in stomach increased
  • Calcium reabsorption in kidney increased (phosphate decreases)
  • Calcium resorption in bone increased
  • Involved in activation of vitamin D (same actions as PTH)
65
Q

What are the 5 main causes of hypercalcaemia?

A
  • Hyperparathyroidism & parathyroid disorders
  • Hypercalcaemia of malignancy
  • Granulomatous lung diseases (tuberculosis and sarcoidosis)
  • Medications (diuretics) & dietary supplements
  • Dehydration
66
Q

What is hypercalcaemia of malignancy?

Why does it occur? 3 reasons

A

Common metabolic abnormality seen in cancer patients

Parathyroid hormone related protein is produced
Local osteolysis
Tumour production of calcitriol

67
Q

Symptoms of hypercalcaemia? Name as many as possible

A

Polydipsia, polyuria, tiredness, headaches, nausea, muscle twitches, kidney stones,

Note: can be asymptomatic

68
Q

3 types of hyperparathyroidism?
How is each treated?
How is a diagnosis made?

A

Primary: increase in PTH due to parathyroid tumour
(1: fluid intake, 2: parathyroidectomy)

Secondary: insufficient vitamin D or renal failure leading to hypocalcaemia and hyperplasia to produce more PTH
(treat cause)

Tertiary: fixed secondary hypocalcaemia, but continued PTH secretion due to hyperplasia
(1: fluid intake, 2: parathyroidectomy)

Dx: calcium and PTH levels, scans - Sestamibi

69
Q

2 types of parathyroid tumour? Which is more common?

A

Parathyroid adenoma: benign tumour, often functional causing primary hyperparathyroidism

Parathyroid carcinoma: rare malignant neoplasm (>1% of parathyroid disease)

70
Q

Cells in the islets of Langerhan:

Names, what they produce, percentage

A

Beta, insulin, 70%
Alpha, glucagon, 20%
Delta, somatostatin, 8%
F?, polypeptide secreting cells

71
Q

Mechanism of insulin secretion?

A

Glucose binds to beta cells
Phosphorylation into glucose-6-phosphate and ATP formed from ADP
K+ channels close, causing depolarisation
Calcium channels open, and influx, causes insulin release

72
Q

3 quantitative diagnostic factors for diabetes mellitus?

What is used for borderline cases?

A 
Random plasma glucose
>11 mmol/L
Fasting plasma glucose
>7 mmol/L
HbA1c
>48 mmol/mol

Impaired glucose tolerance test for borderline cases

73
Q

What is the stress effect on insulin and glucagon by cortisol?

A

Inhibits insulin
Activates glucagon

More glucose available to the body

74
Q

What is the mechanism for type 1 DM?
Associated with which HLA genes?
Inhibited insulin secretion or insulin sensitivity

A

Beta cells express HLA antigens, auto-immune destruction, beta cell loss, impaired insulin secretion

HLA-DR3, HLA-DR4

Impaired insulin secretion

75
Q

Major symptoms of DM?
Type 1 specific?
Is type 2 normally symptomatic?

A

Polydipsia (thirst)
Polyuria/Nocturia (excessive urine)
Glycosuria (glucose in urine)

T1 SPECIFIC:
Weight loss despite polyphagia
Fatigue and irritability

76
Q

What is metabolic syndrome?

Increased risk of…?

A

medical term for a combination of diabetes, high blood pressure (hypertension) and obesity

Stroke and heart disease

77
Q 
KETOACIDOSIS:
Who does it occur in?
Basic mechanism?
3 ketones?
Signs?
Treatment?
A

T1 diabetics

No insulin -> uncontrolled lipolysis -> FFA’s oxidised into ketone bodies

Acetoacetate, Acetone, Beta-hydroxybutyrate

Signs: hypotension, tachycardia, Kussmaul breathing, ketone breath, dehydration

Treatment: rehydration slowly, insulin, replacement of electrolytes

78
Q 
HHS:
What does it stand for?
Who does it occur in?
Mechanism?
Overlap with ketoacidosis? Treatment overlap?
A

Hyperosmolar hyperglycaemic state

Occurs in T2 DM

Dehydration with high glucose concentration in blood, acting as a solute

Does overlap with ketoacidosis, same treatment: rehydration, insulin and replacement of electrolytes

79
Q

How is T1 DM treated?

What are the complications of the major treatment?

A

Education, healthy diet, regular activity, BMI control, BP and hyperlipidaemia control
INSULIN

Complications of insulin therapy:
Hypoglycaemia, lipohypertrophy of injection site, weight gain, insulin resistance, lifestyle issues

80
Q

3 major risk factors for T2 DM?

A

Obesity, physical inactivity, family history

81
Q

Complications of uncontrolled diabetes?

2 categories and examples from each

A

Microvascular: diabetic retinopathy, diabetic nephropathy, diabetic peripheral neuropathy

Macrovascular: CV disease and stroke

82
Q

T2 diabetes control ladder?

A

Lifestyle change

Metformin

Metformin + Sulfonylurea

Metf + Sulf + Insulin (increase as per severity)

83
Q

T2 DM Medications: class, main example, mechanism, side effect, weight gain or loss?

(4)

A

BIGUANIDE: metformin
increases insulin sensitivity and inhibits gluconeogenesis,
sickness and diarrhoea
Weight loss

SULPONHYLUREA: gliclazide
stimulate insulin release by closing K+ pump on beta cells,
hypoglycaemia
Weight gain

DPP4 INHIBITORS: sitagliptin
stimulate incretins (hormones released after eating, which stimulate insulin release)
No weight change

GLITAZONES: pioglitazone
enhance uptake of fatty acids and glucose (more fat made)
Weight gain

84
Q

4 other types of diabetes?

A

Maturity-onset diabetes of the young (MODY)
Gestational diabetes
Drug-induced diabetes
Neonatal diabetes

85
Q

Hypoglycaemia:
Measurement in blood?
Symptoms?
Whipple’s triad?

A

Roughly <3.9mmol/L

Trembling, palpitations, sweating, anxiety, confusion, hunger

Low blood glucose, symptomology, relief after treatment

86
Q

What are carcinoid tumours?
Where are the often found?
Prognosis and signs?
Treatment?

A

Slow growing tumours of neuroendocrine cells (enterochromaffin cells)

Often found in GI tract, also: ovary, testes, bronchi

Bad prognosis, heart failure and bronchoconstriction
Can cause: CARLOAD CRISIS (mediators flood out)

Treatment: octreotide (somatostatin analogue)

87
Q

Two major puberty disorders?

A

Precocious puberty - secondary sexual characteristics appear before 8 y/o in girls and 9 y/o in boys (GNRH dependant or independent)

Delayed puberty -
lack of any pubertal signs by the age of 13 y/o in girls and 14 y/o in boys

88
Q

Tanner stages: boys

A

1 - testicular size increases
2 - sparse pubic hair, increase in testicular size (>3ml)
3 - thicker hair, spreads to mon pubis, penis growth
4 - further enlargement, dark scrotal skin colour, not spreads to medial thighs
5 - adult size and shape, spread to medial surface of thighs

89
Q

Tanner stages: girls

A

1 - no pubic hair, elevation of papilla
2 - breast bud, enlargement of areola, pubic hair
3 - darker, coarse hair, further enlargment
4 - thick adult hair, not spread to thighs, areola and papilla secondary mound
5 - adult size and shape, just papilla projected

Phase 2a (9 decks)

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