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Year 2 > Endocrine Diseases > Flashcards

Endocrine Diseases Flashcards

1
Q

What is diabetes?

What does it result in?

A
  • SIMPLY, IN THE BODIES INABILITY TO REGULATE BLOOD GLUCOSE LEVELS
  • THIS RESULTS IN HYPERGLYCEMIA FROM DEFECT IN INSULIN SECRETION, ACTION OR BOTH
  • LONG TERM, LEADS TO ORGAN DYSFUNCTION, DAMAGE OR FAILURE EG KIDNEYS
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2
Q

What are the main types of diabetes?

A

- TYPE 1- LACK OF INSULIN SECRETION

- TYPE 2- INSULIN INSENSITIVITY - GESTATIONAL- FIRST DIAGNOSED IN PREGNANCY - MODY- AN AD MUTATION RESULTING IN INEFFECTIVE INSULIN PRODUCTION AND SECRETION

  • DIABETES INSIPIDUS
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3
Q

Patho of type 1 diabetes?

Causes?

A
  • TYPE I DIABETES IS A DISORDER THAT RESULTS FROM THE DESTRUCTION OF THE BETA CELLS OF THE PANCREAS, WHICH PRODUCE INSULIN
  • OCCURS IN GENETICALLY SUSCEPTIBLE INDIVIDUALS WITH ENVIRONMENTAL TRIGGER FACTORS, ALTHOUGH THE EXACT AETIOLOGY IS NOT WELL UNDERSTOOD
  • HLA DR3, HLA DR4, HLA DQB1
  • CAN BE TRIGGERED BY A VIRUS
  • AUTOIMMUNE ANTIBODY DESTRUCTION OF BETA CELLS
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4
Q

Ix of Diabetes

Management?

A
  • INVESTIGATIONS: • NO C PEPTIDE • PRESENCE OF ANTIBODIES (ANTI ISLET CELL, ANTI INSULIN, ANTI GAD ETC )
  • PATIENTS REQUIRE LIFE-LONG INSULIN THERAPY AND CARBOHYDRATE COUNTING (FOR DOSE ADJUSTMENTS)
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5
Q

What is DKA?

A

Diabetic ketoacidosis

DKA is a serious acute complications of Diabetes Mellitus - It carries significant risk of death and/or morbidity especially with delayed treatment

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6
Q

Patho of DKA

A
  1. Insulin deficiency causes an increase in blood glucose (hyperglycaemia & glycosuria)
  2. Glycosuria causes an osmotic diuresis leading to water and sodium loss.
  3. The body fails to use glucose as a fuel (insulin is not transporting it into cells)
  4. The body uses fats as a fuel instead, but this leads to ketosis.
  5. An excess of ketone bodies will cause a metabolic acidosis.
  6. Due to the acidosis, K+ ions enter the circulation leading to hyperkalemia
  7. Depending on the duration of DKA, serum K+ may be high, normal or low but the intracellular K+ stores will be depleted.
  8. Phosphate depletion will also occur due to the metabolic acidosis
  9. Na+ loss occurs secondary to the hyperosmotic state
  10. Dehydration can lead to decreased kidney perfusion and acute renal failure
  11. Accumulation of ketone bodies contributes to abdominal pain and vomiting
  12. An increasing acidosis leads to acidotic breathing (Kussmaul) and acetone breath smell (pear drop)
  13. Usually, untreated DKA will lead to impaired consciousness and coma.
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7
Q

Affects of glucagon to DKA

A

Glucagon has no affect. It is catabolic and so it breaks down fats (lipolysis) and protein (loss of muscle mass). High levels of insulin mean fat transported into cells and stored. When there is low levels of insulin fat goes back into the blood from the adipocytes. SO the lack of insulin and normal levels of glucagon causes lots of free FA.

This means there will be lot of free fatty acids in the blood. In the liver the free fatty acids gets converted into ketones. Ketones can be used as energy for cells so they are secreted into blood to go to cells (ketonemia). Can test the ketones In the blood. The ketones also give the sweet smell in breath. Ketones are acids so this causes acidosis (acetoacetic acid and beta hydroxybutyric acid). Remember ketones can only be used slowly and so you can get a build-up of ketones in the blood. The acidosis leads to a diabetic ketoacidosis.

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8
Q

Affects of respiratory centre on DKA

A

The respiratory centre in the medulla oblongata senses the acidosis and causes hyperventilation (rapid deep breathing). Acidosis also causes vasodilation which leads to hypothermia and low blood pressure (hypotension). The hypotension is also from the hyperglycaemia which causes osmotic diuresis which causes hypovolaemia (decreased volume in blood) which causes the low blood pressure. If the hypotension gets worse, it can then lead to shock.

Osmotic diuresis means the patient is losing a lot of fluid which loses a lot of potassium as well (hypokalaemia) which can then cause problems in the heart.

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9
Q

What is DM type 2

A

CAUSED BY A PROGRESSIVE DEFECT IN THE SECRETION OF INSULIN AND ACTION (INSULIN RESISTANCE)

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10
Q

patho of DM type 2

A
  • It usually begins as insulin resistance, a disorder in which the cells do not use insulin properly.
  • As the need for insulin rises, the pancreas gradually loses its ability to produce insulin
  • It is a problem with insulin transport receptors. A reduced amount of these receptors causes blood sugar levels to rise in the blood.
  • to compensate this the pancreas tries to release more insulin so initially there will be a lot of insulin in type 2 but overtime this decreases because the beta cells get tired and so reduction in mass= insulin decrease. (so this is why some people might need insulin if they have type 2)
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11
Q

What are the clinical features of type 1 and type 2

Age

duration of symtoms

body weight

ketonuria

Rapid death

autoantibodies

complication at diagnosis

FHx

other autoimmune diseases

A
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12
Q

Normal glucose physiology?

A

3.5-8mmol per litre

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13
Q

Renal threshold in DM

A

Renal threshold is 11mmol

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14
Q

Three common symptoms of DM

A

Glucosuria, Polyuria, Thirst

  • In the renal tubules, if there is more glucose (more than 11 mmol) then you will have glucose in urine (glycosuria)
  • Glucose attract water so that causes more water to be retained in the urine so that causes more volume of urine (diuresis-abnormally large amount of water being passed).

Weight loss (type1)

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15
Q

What is HbA1c

A

Some glucose while in the blood diffuse into rbc and that attaches to the Hb and this is glycalated glucose. The amount of glucose in the blood is proportional to the amount of glycalated hb. HbA1c is the test to see the amount. The test gives you an average of glucose in the blood over a period of time (8-12 weeks)

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16
Q

Complications of type 1 DM

A

DKA

If glucose levels in brain will be low- if too low then you can go into acute hypoglycaemic coma. This happens if we give too much insulin without any food intake because glucose levels would already be low so you would be lowering it further.

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17
Q

THE FOUR MAIN DETERMINING FACTORs of DM type 2

A

AGE, OBESITY, FAMILY HISTORY AND ETHNICITY

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18
Q

there is no association between HLA and type 2 DM

true or false

A

True

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19
Q

WHat is HHS?

A

Diabetic hyperglycemic hyperosmolar syndrome (HHS) is a complication of type 2 diabetes. It involves extremely high blood sugar (glucose) level without the presence of ketones.

HYPERGLYCAEMIA WITHOUT KETONES OR ACIDOSIS.

  • VERY SIMILAR PATHOPHYSIOLOGY TO DKA, BUT THE INSULIN DEFICIENCY IS NOT ENOUGH TO CAUSE KETOGENESIS AND LIPOLYSIS.
  • SAME MANAGEMENT AS DKA
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20
Q

WHat to look out for if the patient has HHS?

A

PATIENT WITH UNDIAGNOSED DIABETES, NEWLY DIAGNOSED PATIENT, PATIENT WHO DOES NOT TAKE INTEREST IN THEIR HEALTH, ANYTHING LEADING YOU TO THINK THEY DO NOT TAKE THEIR MEDICATION

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21
Q

Hypothyroidism

common in men or women?

A

older women

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22
Q

What is the difference between primary and secondary cause of hypthyroidism?

A
  • Primary- cause within the thyroid gland - Failure to produce enough T4/T3
  • Secondary- cause within the pituitary/ hypothalamus (central) - Failure to produce enough TSH
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23
Q

Causes for Hypothyroidism?

A
  • AI thyroiditis: Hashimoto’s- Anti-TPO antibodies , Atrophic
  • Drugs eg lithium, amiodarone
  • Secondary to treatment of hyperthyroidism
  • Congenital (1 in 3500 births)
  • Iodine deficiency
  • Pituitary adenoma
  • Surgery/ radiotherapy
  • Head trauma
  • Vascular- Sheehan’s syndrome
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24
Q

Treatment for hypothyroidism

A

• Levothyroxine • Synthetic T4 • Titrated until TSH levels are normal

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25
Q

What is myxoedema Coma?

A
  • Severe and life-threatening medical emergency
  • Occurs in people with poorly controlled hypothyroidism who are undergoing a stressful event (surgery or infection)
  • Features- altered consciousness, confusion, hypothermia, bradycardia, hypotension and accumulation of drugs
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26
Q

What is hyperthyroidism?

Primary?

Secondary?

A
  • Excessive production of thyroid hormone
  • Primary- problem with thyroid gland
  • Secondary- problem with pituitary/ hypothalamus
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27
Q

Causes of hyperthyroidism?

A
  • Graves disease
  • Toxic multinodular goitre
  • Hashimoto’s thyroiditis
  • Toxic adenoma
  • Drugs- amiodarone, iodine
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28
Q

WHat is thyrotoxicosis?

A

thyrotoxicosis is the clinical manifestation of excess thyroid hormone action at the tissue level due to inappropriately high circulating thyroid hormone concentrations.

Hyperthyroidism, a subset of thyrotoxicosis, refers specifically to excess thyroid hormone synthesis and secretion by the thyroid gland

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29
Q

Causes of thyrotoxicosis

A
  • Exogenous thyroid hormones
  • Subacute thyroiditis
  • Ectopic thyroid tissue
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30
Q

Hyperthyroidism

symptoms?

A
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31
Q

What is Graves Disease

A

Graves’ disease (aka toxic diffuse goitre) is an autoimmune disease that affects the thyroid. - It frequently results in and is the most common cause of hyperthyroidism. - It also often results in an enlarged thyroid.

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32
Q

Patho of graves

A
  • TRAb Antibodies bind to and stimulate the TSH receptors producing excessive thyroid hormone and thyroid enlargement
  • More common in women
  • Associated with T1DM and Addison’s
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33
Q

What are the three unique features of graves?

A
  • Graves Opthalmopathy (Exophthalmos, periorbital oedema, scleral infections, optic neuropathy, lid lag)
  • Graves dermopathy (pretibial myxoedma)
  • Thyroid acropachy - digital clubbing, soft tissue swelling of the hands and feet, and periosteal new bone formation.
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34
Q

What is the first line of management for graves/hyperthyroidism?

second line

A

Carbimazole (reduces thyroid hormone synthesis)

• Propylthiouracil is the second line anti-thyroid drug. It is used in a similar way to carbimazole. There is a small risk of severe hepatic reactions, including death, which is why carbimazole is preferred.

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35
Q

Management of symtoms for hyperthyroidism?

A

Beta blockers eg propanolol

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36
Q

What is thyroid storm?

A
  • Medical emergency due to exacerbation of severe thyrotoxicosis
  • Causes by stressful events eg infection and surgery

Thyroid storm is a very rare, but life-threatening condition of the thyroid gland that develops in cases of untreated thyrotoxicosis (hyperthyroidism, or overactive thyroid). The thyroid gland is located in the neck, just above where your collarbones meet in the middle.

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37
Q

clinical features and management for thyroid storm?

A
  • Clinical features: severe hyperthyroidism, hyperpyrexia, altered mental state, tachycardia, cardiac failure, jaundice/abdo pain
  • Managed via anti-thyroid drugs, potassium iodide, beta-blockers, steroids
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38
Q

Most common type of thyroid cancer?

A

Papillary (80%)

Follicular (10%)

Medullary (5%)

ANaplastic (rare)

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39
Q

Which type of thyroid cancer happens in all ages?

A

papillary

40
Q

Which thyroid cancer arise from parafollicular cells?

A

Medullary

41
Q

Label A-E

A

A - Progesterone

B - Aldosterone
C - Cortisol
D - Testosterone
E - Estradiol

42
Q

What is the effects of cortisol in:

Liver

Muscle

Adipose tissue

Immune system

CNS

Increases ADH production

A
43
Q

Cushings syndrome vs Cushing’s disease

A
  • Cushing syndrome: constellation of symptoms associated with cortisol excess
  • Cushing’s disease: Cushing’s syndrome due to pituitary ACTH hypersecretion (secondary)
44
Q

Causes of Cushing syndrome?

A
  • Pituitary (65%)
  • Adrenal (25%)
  • adrenal adenoma
  • Ectopic source (small cell lung cancer, ACTH producing tumour) 10%
  • Exogenous cause e.g. steroids (asthma, RA)
45
Q

How do you remember the symptoms of CUSHING’s syndrome and what are they?

A

SWEDISH

  • Spinal tenderness/ osteoporosis
  • Weight gain
  • Easily bruise
  • Diabetes (type 2)
  • Intracapsular fat pad
  • Striae
  • Hypertension
46
Q

This is an example of

A

Cushing’s syndrome

47
Q

What are the differentilas for Cushings

A
  • Obesity
  • Poorly controlled diabetes
  • Excess alcohol consumption
  • Chronic anxiety and depression
48
Q

What is the first line bochemical tests for cushings?

A
  • Urine free cortisol (UFC)
  • 1mg overnight Dexamethasone Suppression test (ODST)- If cortisol is high (>50nmol/L): Cushing’s syndrome
  • 8mg High dose dexamethasone suppression test - If cortisol is low: Pituitary adenoma (Cushing’s disease)
  • Plasma ACTH - If high: Ectopic ACTH - If low: adrenal adenoma (independent of ACTH)
49
Q

What is another name for hyperaldostronism

A

Conn’s syndrome

50
Q

What is Primary Hyperaldosteronism (Conn’s syndrome)

A
  • Adrenal glands produce too much aldosterone (independent of RAAS)
  • Adrenal adenoma (most common)
  • Bilateral adrenal hyperplasia
  • Familial hyperaldosteronism type 1 and 2
  • Adrenal carcinoma
51
Q

What is - Secondary Hyperaldosteronism

A
  • Excessive renin stimulates the adrenal gland to produce more aldosterone (activated by RAAS)
  • Blood pressure in kidney is low
  • Renal artery stenosis/obstruction
  • Heart failure
  • Pregnancy: oestrogen-induced increase in renin
52
Q

what is the common cause of Conn’s syndrome?

A
  • Hypertension because

Excess aldosterone → increase blood pressure → suppress RAAS, decreased renin

53
Q

Complications of conns syndrome

A
  • Hypertension lead to heart disease, stroke and intracerebral haemorrhage
  • Hypokalaemia (secretion of K+) - cardiac arrhythmias
54
Q

Ix for Hyperaldosteronism

A
  • Renin:aldosterone ratio - High aldosterone and low renin: Primary hyperaldosteronism - High aldosterone and high renin: secondary hyperaldosteronism
  • Other investigations - Blood pressure - Serum electrolytes (hypokalaemia) - Blood gas analysis (alkalosis)
  • Investigate or cause - CT/MRI to look for adrenal tumour - Renal doppler USS, CT angiogram or MR angiogram for renal artery stenosis or obstruction
55
Q

What is adrenal insufficiency?

A
  • Adrenal insufficiency: adrenal glands do not produce enough steroid hormones particularly cortisol and aldosterone
  • Primary adrenal insufficiency: Addison’s disease - adrenal glands have been damaged
  • Secondary adrenal insufficiency: Inadequate ACTH stimulating adrenal glands due to damage or loss of pituitary gland
56
Q

Does Addison’s disease affect more women or men

A

women

57
Q

Ix addisons

A
  • UEs
  • Early morning cortisol
  • Short synacthen test (gold standard) - ACTH stimulation test
  • ACTH
  • Adrenal autoantibodies: adrenal cortex antibodies and 21-hydroxylase antibodies
  • CT/MRI adrenals
  • adrenal tumour, haemorrhage
  • MRI pituitary
58
Q

What is Addisonian crisis?

A

An Addisonian crisis is a serious medical condition caused by the body’s inability to produce a sufficient amount of cortisol. An Addisonian crisis is also known as an acute adrenal crisis

Acute presentation of severe Addison’s, where the absence of steroid hormones leads to a life threatening presentation:

59
Q
A
60
Q
A
61
Q

Examples of pituitary tumours

A

Functioning adenomas

non functioning adenomas

62
Q

Examples of function adenomas

A

Acromegaly

Cushings

Prolactinoma

TSHoma

63
Q

Examples of non functioning adenomas

A

Null cell adenomas

Gonadotroph adeomas

clinically silent adenomas

64
Q

What are other causes of pituitary dysfunction

A

Pituitary apoplexy

Cranial Radiotherapy

Surgical induced

Traumatic brain injury

Late effects of cancer treamtent

Postpartum necrosis

Inflammatory conditions

Genetic causes

65
Q

What is the most common pituitary adenoma?

A

Prolactinoma

66
Q

Main clinical features of prolactinoma?

A
  • Galactorrhoea, menstrual disturbances
  • Low libido and erectile dysfunction
  • Compression effects for macroadenomas (bitemporal hemianopia)
67
Q

Diagnosis of pituitary adenoma

A
  • Rule out any secondary causes first
  • Measure prolactin, prolactin will be raised, FSH and LH will be low as prolactin inhibits GnRH secretion
  • Macroadenomas; > 5000 U/L
  • MRI pituitary is useful
68
Q

Treatment for prolactinoma?

A
  • Dopamine agonists (bromocriptine, cabergoline)- as dopamine will inhibit prolactin. Side effects include: Constipation; drowsiness; headache; nasal congestion; nausea
  • Surgical resection if medication not tolerated
69
Q

What is acromegaly?

A
  • Elevated GH
  • Most commonly due to a benign pituitary adenoma/ hyperplasia • There will also be increased IGF-1 levels
  • Commonly diagnosed between ages 30-50
70
Q

Acromegaly symptoms?

A
  • Headache, sweating, clothes and hat fit tightly
  • Amenorrhoea
  • Deep voice and slow speech
71
Q

What do you see on physcial examination for acromegaly?

A
  • Hypertension
  • Enlarged head with frontal bossing and deepened facial folds
  • Enlarged fingers and feet
  • Enlarged jaw with increased teeth spacing
  • Neuropathy and muscle weakness
72
Q

Acromegaly diagnosis

Ix

diagnosis?

A

Investigations

•\ Baseline pituitary profile • GH levels and IGF-1 • Renal, liver, lipids, glucose function • ECG, ECHO, CXR

Diagnosis

  1. Measure GH after oral glucose tolerance test 2. If GH > 1 µg/L usually diagnostic 3. Raised IGF-1 is also helpful 4. Pituitary MRI
73
Q

What is diabetes inspidua?

A

• Large volumes of dilute urine often >3L per day • Due to insufficient ADH production in posterior pituitary gland , so unable to concentrate urine

74
Q

treatment for diabetes inspidus

A

• With the water deprivation test, the urine osmolarity will be low to start with, but as the desmopressin is given, the urine osmolarity will increase again. • Treatment; Desmopressin (ADH analogue)

75
Q

Clinical Features of hypercalcemia

A
  • Lethargy and general aches
  • Polyuria, polydipsia
  • Anorexia, nausea, vomiting
  • Dehydration
  • Constipation
  • Psychosis
  • Bradycardia and heart block
  • Kidney failure
76
Q

What is Primary Hyperparathyroidism

A
  • Most common cause of raised calcium , can be caused by an adenoma/hyperplasia in the parathyroid gland
  • Hypercalcemia- increased kidney stone risk
  • Excessive bone resorption; can be associated with -Osteoporosis, fracture risk -Subperiosteal resorption - Osteitis fibrosa cystica; cystic bone spaces with brown fibrous tissue
77
Q
A
78
Q

Treatment of hypercalcemia

A

Stop calcium, vitamin D

Oral fluids

IV normal saline ( if > 3 mmol/L)

Antiresorptives which will inhibit osteoclastic activity ie bisphosphonate

79
Q

What are MAJOR causes of Hypocalcaemia?

A

sepsis, hypomagnesaemia, hypoparathyroidism and vitamin D deficiency

80
Q

What is pathology CAH- congenital adrenal hyperplasia

A
  • CAH (congenital adrenal hyperplasia) refers to a group of conditions characterized by a defect in the enzymes involved in the synthesis of adrenal steroids, particularly cortisol
  • Beta 21 hydroxylase deficiency (enzyme)
  • Impaired aldosterone production= salt loss
81
Q

CAH- congenital adrenal hyperplasia Clinical features?

A
  • Reduced cortisol production - Impaired glucose metabolism
  • Increased ACTH= hyperpigmentation of the skin
  • Increased androgens= secondary sexual characteristics - Females: - Pseudo hirsutism - Clitoral hypertrophy
  • Male secondary sexual characteristics - Males: - Early puberty- precocious puberty in males -

**there may be a decreased production of aldosterone: - Salt loss - Hypotension - Dizziness

  • Life- threatening in neonates - Suspect in any neonate with ambiguous genitalia - In females: exclude androgen secreting ovarian neoplasm
82
Q

CAH- congenital adrenal hyperplasia

management

A
  • Glucocorticoid replacement - IV hydrocortisone
  • Mineralocorticoid replacement - Fludrocortisone
  • Glucose
  • IV fluids
  • Surgery- surgical correction of external genitalia
  • If identified during pregnancy🡪 dexamethasone is given
83
Q

Pathology of Pheochromocytoma

A
  • It is an adrenal medullary tumour
  • Increased production of epinephrine, norepinephrine (chromaffin cells)
  • Associated with genetic conditions such as: - Familial pheochromocytoma - Neurofibromas - Multiple endocrine neoplasia (MEN type 2)
84
Q

Pheochromocytoma

CF

A
  • Headache - Sweat - Tachycardia - Palpitations - Tremor - Orthostatic hypotension - Cardiomyopathy- due to catecholamines
85
Q

Pheochromocytoma

Investigations

A
  • Urine and plasma: metanephrine and normetanephrine
  • MIBG scan
  • USS scan of kidneys
  • Rule out hyperthyroidism and hyperaldosteronism
86
Q

Pheochromocytoma

Management

A
  • Adrenalectomy - Blood pressure control: alpha blocker🡪 beta blocker. - CCB may be used as add on treatment
87
Q

What is MEN

A

Multiple endocrine neoplasia

  • Ten to affect multiple endocrine organs - Even within the same endocrine organ, tend to be multifocal - Cause C cell hyperplasia of the the thyroid - Occur in a younger age group
88
Q

How many types of MEN are there?

A

MEN type1

MEN type 2 IIa IIb

89
Q

What is MEN type 1

A
  • Pancreas ( Zollinger- Ellison , pituitary (prolactinoma), parathyroid
  • Autosomal dominant
  • Primary hyperparathyroidism 🡪 most common manifestation
90
Q

MEN type 2

A
  • Activate mutations in the RET proto-oncogene
  • Two types: MEN Type IIa, MEN type IIb
91
Q

MEN Type IIa

A
  • Thyroid- 50+ age group) - Familial thyroid carcinoma (50+ age group) - Medullary thyroid cancer – poor prognosis
  • Adrenal - Adrenal pheochromocytoma - 10% malignant
  • Parathyroid - 10-20% - Hyperparathyroidism
92
Q

MEN Type IIb

A
  • No primary hyperparathyroidism
  • Associated with ganglioneuromas of stomach, lips, tongue etc.- oral/intestinal neuromas
  • Marfanoid syndrome: long length of axial skeleton🡪 impression of Marfan syndrome
93
Q

Paraganglioma Patholgy

A
  • Extra-adrenal tumors • Chromaffin cell tumour in adrenal medulla= pheochromocytoma • Chromaffin cell tumors elsewhere in the body= paragangliomas
  • chromaffin cells🡪 may secrete catecholamines • Derived form sympathetic paravertebral ganglion
  • Increased risk of malignancy
  • Age- 30-50 years
94
Q

Paraganglioma

TYpes

A
  • Sympathetic paragangliomas • Found adjacent to the sympathetic paravertebral ganglia (pelvis, abdomen and the thorax • Secrete catecholamines • Mimic symptoms of pheochromocytoma
  • Parasympathetic paragangliomas • Located alongside vagal nerve, glossopharyngeal nerve • Non-functional
95
Q

Paraganglioma

Diagnosis

A
  • Serum and urine metanephrine/ catecholamines
  • Tumor marker: Chromogranin A
  • Imaging: MIBG, MRI, CT
  • Genetic testing
96
Q

Paragangliom a

Treatment

A
  • operative: resection of the paraganglioma tumor
  • Alpha blockers🡪 beta blockers - CCB may be used
  • Radiation therapy- stereotactic body radiotherapy (focused radiotherapy on the tumor- minimal risk of damage to adjacent healthy tissue)

Year 2 (33 decks)

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