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Pathoma > Endocrine Pathology > Flashcards

Endocrine Pathology Flashcards

1
Q

Benign tumor of anterior pituitary cells
May be functional (hormone-producing) or nonfunctional (silent)
1. Nonfunctional tumors often present with mass effect.
i. Bitemporal hemianopsia occurs due to compression of the optic chiasm
ii. Hypopituitarism occurs due to compression of normal pituitary tissue
iii. Headache
Functional tumors present with features based on the type of hormone produced.
Prolactinoma presents as galactorrhea and amenorrhea (females) or as decreased
libido and headache (males); most common type of pituitary adenoma
Growth hormone cell adenoma
1. Gigantism in children - increased linear bone growth (epiphyses are not fused)
2. Acromegaly in adults
i. Enlarged bones of hands, feet, and jaw
ii. Growth ofvisceral organs leading to dysfunction (e.g., cardiac failure) iii. Enlarged tongue
3. Secondary diabetes mellitus is often present (GH induces liver gluconeogenesis)
4. Diagnosed by elevated GH and insulin growth factor-1 (IGF-1) levels along with lack of GH suppression by oral glucose
5. Treatment is octreotide (somatostatin analog that suppresses GH release), GH
receptor antagonists, or surgery.
ACTH cell adenomas secrete ACTH leading to Cushing syndrome
F. TSH cell, LH-producing, and FSH-producing adenomas occur, but are rare
What condition could this be

A

Pituitary adenoma

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2
Q

How does prolactinoma present

A

Galactorrhea
Amenorrhea (females)
Decreased libido and headache (males); most common type of pituitary adenoma

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3
Q

How is prolactinoma treated

A

Dopamine agonists (e.g., bromocriptine or cabergoline) to suppress prolactin production (shrinks tumor)
Surgery for larger lesions

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4
Q

How does acromegaly manifest in adults

A

Enlarged bones of hands, feet, and jaw
Growth of visceral organs leading to dysfunction (e.g., cardiac failure)
Enlarged tongue

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5
Q

How is pituitary adenoma diagnosed

A

Diagnosed by elevated GH and insulin growth factor-1 (IGF-1) levels along with lack of GH suppression by oral glucose

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6
Q

What are some causes of hypopituitarism

A

Pituitary adenomas (adults) or craniopharyngioma (children) - due to mass effect or pituitary apoplexy (bleeding into an adenoma)
Sheehan syndrome - pregnancy-related infarction of the pituitary gland
i. Gland doubles in size during pregnancy, but blood supply does not increase significantly; blood loss during parturition precipitates infarction.
ii. Presents as poor lactation, loss of pubic hair, and fatigue
Empty sella syndrome-congenital defect of the sella
i. Herniation of the arachnoid and CSF into the sella compresses and destroys the pituitary gland.
ii. Pituitary gland is “absent” (empty sella) on imaging

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7
Q

……… and …….. are made in the hypothalamus and then
transported via axons to the posterior pituitary for release.

A

ADH, oxytocin

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8
Q

What’s the function of ADH

A

ADH acts on the distal tubules and collecting ducts of the kidney to promote free water retention

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9
Q

What is the function of oxytocin

A

Oxytocin mediates uterine contraction during labor and release of breast milk (let-down) in lactating mothers

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10
Q

Cystic dilation of thyroglossal duct remnant
1. Thyroid develops at the base of tongue and then travels along the thyroglossal duct to the anterior neck.
2. Thyroglossal duct normally involutes; a persistent duct, however, may undergo cystic dilation.
Presents as an anterior neck mass
What condition could this be

A

Thyroglossal duct cyst

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11
Q

Persistence of thyroid tissue at the base of tongue
Presents as a base of tongue mass
What condition could this be

A

Lingual thyroid

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12
Q

What are some clinical features of hyperthyroidism

A

Weight loss despite increased appetite
Heat intolerance and sweating
Tachycardia with increased cardiac output
Arrhythmia (e.g., atrial fibrillation), especially in the elderly
Tremor, anxiety, insomnia, and heightened emotions
Staring gaze with lid lag
Diarrhea with malabsorption
Oligomenorrhea
Bone resorption with hypercalcemia (risk for osteoporosis)
Decreased muscle mass with weakness
Hypocholesterolemia
Hyperglycemia (due to gluconeogenesis and glycogenolysis)

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13
Q

What is hyperthyroidism

A

Increased level of circulating thyroid hormone
1. Increases basal metabolic rate (due to increased synthesis of Na+-K+ ATPase)
2. Increases sympathetic nervous system activity (due to increased expression of β1-adrenergic receptors)

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14
Q

What are some clinical features of Grave’s disease

A

Hyperthyroidism
Diffuse goiter - Constant TSH stimulation leads to thyroid hyperplasia and hypertrophy

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15
Q

What is the most common cause of hyperthyroidism

A

Graves’ disease

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16
Q

Autoantibody (IgG) that stimulates TSH receptor (type II hypersensitivity)
Leads to increased synthesis and release of thyroid hormone
1. Most common cause of hyperthyroidism
2. Classically occurs in women of childbearing age (20-40 years)
Clinical features include Hyperthyroidism and diffuse goiter - constant TSH stimulation leads to thyroid hyperplasia and
hypertrophy
3. Exophthalmos and pretibial myxedema
i. Fibroblasts behind the orbit and overlying the shin express the TSH receptor
ii. TSH activation results in glycosaminoglycan (chondroitin sulfate and hyaluronic acid) buildup, inflammation, fibrosis, and edema leading to exophthalmos and pretibial myxedema
What condition could this be

A

Graves’ disease

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17
Q

What are the laboratory findings in Graves’ disease

A
  1. ↑ total and free T4; ↓ TSH (free T3 downregulates TRH receptors in the anterior pituitary to decrease TSH release)
  2. Hypocholesterolemia
  3. Increased serum glucose
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18
Q

What the treatment for Graves’ disease

A

β- blockers
Thioamide
Radioiodine ablation

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19
Q

What is a potential fatal complication for Graves’ disease

A

Thyroid storm
1. Due to elevated catecholamines and massive hormone excess, usually in response to stress (e.g., surgery or childbirth)
2. Presents as arrhythmia, hyperthermia, and vomiting with hypovolemic shock
3. Treatment is propylthiouracil (PTU), β- blockers, and steroids.
i. PTU inhibits peroxidase-mediated oxidation, organification, and coupling steps of thyroid hormone synthesis, as well as peripheral conversion o f T4 to T3

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20
Q

What could cause a thyroid storm in Graves’ disease

A

Due to elevated catecholamines and massive hormone excess, usually in response
to stress (e.g., surgery or childbirth)
Presents as arrhythmia, hyperthermia, and vomiting with hypovolemic shock
Treatment is propylthiouracil (PTU), β- blockers, and steroids.
i. PTU inhibits peroxidase-mediated oxidation, organification, and coupling steps of thyroid hormone synthesis, as well as peripheral conversion o f T4 to T3

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21
Q

How do you treat a thyroid storm in Graves’ disease

A

Propylthiouracil (PTU)
β- blockers
Steroids

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22
Q

What are some types of hypothyroidism

A

Cretinism
Myxedema

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23
Q

Hypothyroidism in neonates and infants
Characterized by mental retardation, short stature with skeletal abnormalities, coarse facial features, enlarged tongue, and umbilical hernia
What condition could this be

A

Cretinism

1. Thyroid hormone is required for normal brain and skeletal development.
Causes include maternal hypothyroidism during early pregnancy, thyroid agenesis,
dyshormonogenetic goiter, and iodine deficiency.
1. Dyshormonogenetic goiter is due to a congenital defect in thyroid hormone production; most commonly involves thyroid peroxidase

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24
Q

What are some clinical features of myxedema

A

Clinical features are based on decreased basal metabolic rate and decreased sympathetic nervous system activity
1. Myxedema - accumulation of glycosaminoglycans in the skin and soft tissue
Results in a deepening of voice and large tongue
Weight gain despite normal appetite
Slowing of mental activity
Muscle weakness
Cold intolerance with decreased sweating
Bradycardia with decreased cardiac output, leading to shortness of breath and fatigue
Oligomenorrhea
Constipation
Hypercholesterolemia

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25
Q

What are the most common causes of myxedema

A

Iodine deficiency and Hashimoto thyroiditis
Other causes include drugs (e.g., lithium)
Surgical removal or radioablation of the thyroid

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26
Q

What are the various types of thyroiditis

A

Hashimoto thyroiditis
Subacute granulomatous (De Quervain) thyroiditis
Riedel fibrosing thyroiditis

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27
Q

What are some clinical features of Hashimoto thyroiditis

A

Initially may present as hyperthyroidism (due to follicle damage)
Progresses to hypothyroidism; ↓T4 and↑TSH
Antithyroglobulin and antithyroid peroxidase antibodies are often present (sign of thyroid damage)

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28
Q

Autoimmune destruction of the thyroid gland; associated with HLA-DR5
1. Most common cause of hypothyroidism in regions where iodine levels are adequate
Chronic inflammation with germinal centers and Hurthle cells (eosinophilic
metaplasia of cells that line follicles) is seen on histology
Increased risk for B-cell (marginal zone) lymphoma; presents as an enlarging thyroid gland late in disease course
What condition could this be

A

Hashimoto thyroiditis

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29
Q

Granulomatous thyroiditis that follows a viral infection
Presents as a tender thyroid with transient hyperthyroidism
Self-limited; rarely (15% of cases) may progress to hypothyroidism
What condition could this be

A

Subacute granulomatous thyroiditis

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30
Q

Chronic inflammation with extensive fibrosis of the thyroid gland
Presents as hypothyroidism with a ‘hard as wood,’ nontender thyroid gland
Fibrosis may extend to involve local structures (e.g., airway).
1. Clinically mimics anaplastic carcinoma, but patients are younger (40s), and malignant cells are absent
What condition could this be

A

Riedel fibrosing thyroiditis

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31
Q

Usually presents as a distinct, solitary nodule
1. Thyroid nodules are more likely to be benign than malignant.
131 I radioactive uptake studies are useful to further characterize nodules.
1. Increased uptake (‘hot’ nodule) is seen in Graves disease or nodular goiter.
2. Decreased uptake (‘cold’ nodule) is seen in adenoma and carcinoma; often warrants biopsy
Biopsy is performed by fine needle aspiration (FNA)
What condition could this be

A

Thyroid neoplasia

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32
Q

Benign proliferation of follicles surrounded by a fibrous capsule
Usually nonfunctional; less commonly, may secrete thyroid hormone
What condition could this be

A

Follicular adenoma

33
Q

What is the most common type of thyroid carcinoma (80% of cases)

A

Papillary carcinoma

34
Q

Most common type of thyroid carcinoma (80% of cases)
Exposure to ionizing radiation in childhood is a major risk factor
Comprised of papillae lined by cells with clear, ‘Orphan Annie eye’ nuclei and nuclear grooves; papillae are often associated with psammoma bodies
Often spreads to cervical (neck) lymph nodes, but prognosis is excellent (10-year survival> 95%)
What condition could this be

A

Papillary carcinoma

35
Q

Malignant proliferation of follicles surrounded by a fibrous capsule with invasion through the capsule (invasion through the capsule helps distinguish follicular carcinoma from
follicular adenoma. Entire capsule must be examined microscopically)
3. FNA only examines cells and not the capsule; hence, a distinction between
follicular adenoma and follicular carcinoma cannot be made by FNA.
Metastasis generally occurs hematogenously
What condition could this be

A

Follicular carcinoma

36
Q

Calcitonin often deposits within the tumor as

A

Amyloid

37
Q

What are C cells

A

C cells are neuroendocrine cells that secrete calcitonin
Calcitonin lowers serum calcium by increasing renal calcium excretion but is inactive at normal physiologic levels
High levels of calcitonin produced by tumor may lead to hypocalcemia
Calcitonin often deposits within the tumor as amyloid

38
Q

What is a medullary carcinoma

A

Malignant proliferation of parafollicular C cells; comprises 5% of thyroid carcinomas
Familial cases are often due to multiple endocrine neoplasia (MEN) 2A and 2B, which are associated with mutations in the RET oncogene.
1. MEN 2 results in medullary carcinoma, pheochromocytoma, and parathyroid adenomas (2A) or ganglioneuromas of the oral mucosa (2B)
2. Detection of the RET mutation warrants prophylactic thyroidectomy

39
Q

Undifferentiated malignant tumor of the thyroid; usually seen in elderly
Often invades local structures, leading to dysphagia or respiratory compromise
Poor prognosis
What condition could this be

A

Anaplastic carcinoma

40
Q

What is the use of parathyroid hormone

A

Chief cells regulate serum free (ionized) calcium via parathyroid hormone (PTH) secretion, which
1. Increases bone osteoclast activity, releasing calcium and phosphate
2. Increases small bowel absorption of calcium and phosphate (indirectly by
activating vitamin D)
3. Increases renal calcium reabsorption (distal tubule) and decreases phosphate reabsorption (proximal tubule)
Increased serum ionized calcium levels provide negative feedback to decrease PTH secretion

41
Q

Which cells regulate free ionized calcium via PTH secretion

A

Chief cells

42
Q

What are the lab findings for primary hyperparathyroidism

A

Laboratory findings include
↑serum PTH
↑serum calcium
↑urinary cAMP
↑serum alkaline phosphatase
↓serum phosphate

43
Q

What is the treatment for primary hyperparathyroidism

A

Treatment involves surgical removal of the affected gland

44
Q

What are some clinical features of primary hyperparathyroidism

A

Most often results in asymptomatic hypercalcemia; however, may present with consequences of increased PTH and hypercalcemia such as
i. Nephrolithiasis (calcium oxalate stones)
ii. Nephrocalcinosis - metastatic calcification of renal tubules, potentially leading to renal insufficiency and polyuria
iii. CNS disturbances (e.g., depression and seizures)
iv. Constipation, peptic ulcer disease, and acute pancreatitis
v. Osteitis fibrosa cystica - resorption of bone leading to fibrosis and cystic spaces

45
Q

Excess PTH due to a disorder o f the parathyroid gland itself
Most common cause is parathyroid adenoma (>80% of cases); sporadic parathyroid hyperplasia and parathyroid carcinoma are less common causes
What condition could this be

A

Primary hyperparathyroidism

46
Q

Excess production of PTH due to a disease process extrinsic to the parathyroid gland
Most common cause is chronic renal failure
Renal insufficiency leads to decreased phosphate excretion.
2. ↑ serum phosphate binds free calcium.
3. ↓ free calcium stimulates all four parathyroid glands.
4. ↑ PTH leads to bone resorption (contributing to renal osteodystrophy)
What condition could this be

A

Secondary hyperparathyroidism

47
Q

What are the lab findings in secondary hyperparathyroidism

A

↑PTH
↑serum phosphate
↑alkaline phosphatase.
↓serum calcium

48
Q

What are the function of the layers of the adrenal cortex

A

Glomerulosa produces mineralocorticoids (e.g., aldosterone).
Fasciculata produces glucocorticoids (e.g., cortisol).
Reticularis produces weak androgens (e.g., DHEA)

49
Q

Excess aldosterone
Classically presents as HTN, hypokalemia, and metabolic alkalosis
1. Aldosterone increases absorption of sodium and secretion of potassium and hydrogen ions in the distal tubule and collecting duct.
2. Increased sodium expands plasma volume leading to HTN
Primary hyperaldosteronism is most commonly due to bilateral adrenal hyperplasia (60%) or adrenal adenoma (40%, Conn syndrome); adrenal carcinoma is rare.
1. CT is useful to determine pathology
2. Treatment for bilateral adrenal hyperplasia is mineralocorticoid receptor antagonist (e.g., spironolactone or eplerenone); adenoma and carcinoma are
surgically resected.
Secondary hyperaldosteronism arises with activation of the renin angiotensin system (e.g., renovascular hypertension or CHF)
What condition could this be

A

Hyperaldosteronism

50
Q

Primary hyperaldosteronism is most commonly due to

A

Bilateral adrenal hyperplasia or adrenal adenoma; adrenal carcinoma is rare

51
Q

What is the investigation for hyperaldosteronism

A

CT

52
Q

What is the treatment for bilateral adrenal hyperplasia

A

Treatment for bilateral adrenal hyperplasia is mineralocorticoid receptor antagonist (e.g., spironolactone or eplerenone); Adenoma and carcinoma are
surgically resected

53
Q

What are some clinical features of hyperaldosteronism

A

HTN
Hypokalemia
Metabolic alkalosis

54
Q

How are primary and secondary hyperaldosteronism distinguished

A

Primary and secondary hyperaldosteronism are distinguished by plasma renin and edema
1. Primary is characterized by low renin and no edema (aldosterone escape)
2. Secondary is characterized by high renin; edema is often present

55
Q

Which syndromes mimic hyperaldosteronism

A

Liddle syndrome
Decreased degradation of sodium channels in collecting tubules due to genetic mutation; autosomal dominant
Presents as child with HTN, hypokalemia, and metabolic alkalosis, but with low aldosterone and low renin
Diagnosed by genetic testing
Treatment is potassium-sparing diuretics (e.g., amiloride or triamterene), which block tubular sodium channels; spironolactone is not effective

Syndrome of apparent mineralocorticoid excess (SAME)
1. 11β- hydroxysteroid dehydrogenase 2 (11β- HSD2) deficiency allows cortisol to activate renal aldosterone receptors; autosomal recessive
2. Presents as child with HTN, hypokalemia, and metabolic alkalosis, but with low aldosterone and low renin
3. Diagnosed by low urinary free cortisone and genetic testing
4. May also arise with licorice (glycyrrhetinic acid), which blocks 11β- HSD2

56
Q

How is Liddle syndrome treated

A

Treatment is potassium-sparing diuretics (e.g., amiloride or triamterene), which block tubular sodium channels; spironolactone is not effective

57
Q
  1. 11β- hydroxysteroid dehydrogenase 2 (11β- HSD2) deficiency allows cortisol to activate renal aldosterone receptors; autosomal recessive
  2. Presents as child with HTN, hypokalemia, and metabolic alkalosis, but with low aldosterone and low renin
  3. Diagnosed by low urinary free cortisone and genetic testing
  4. May also arise with licorice (glycyrrhetinic acid), which blocks 11β- HSD2
    Which condition could this be
A

Syndrome of apparent mineralocorticoid excess (SAME)

58
Q

What are some clinical features of hypercortisolism

A
  1. Muscle weakness with thin extremities - Cortisol breaks down muscle to produce amino acids for gluconeogenesis
  2. Moon fades, buffalo hump, and truncal obesity - High insulin (due to high glucose) increases storage of fat centrally
  3. Abdominal striae - Impaired collagen synthesis results in thinning of skin
  4. HTN often with hypokalemia and metabolic alkalosis
    i. High cortisol increases sensitivity of peripheral vessels to catecholamines. ii. At very high levels, cortisol cross-reacts with mineralocorticoid receptor (aldosterone is not increased).
  5. Osteoporosis
  6. Immune suppression
59
Q

How is hypercortisolism diagnosed

A

Diagnosis is based on 24-hour urine cortisol level (increased), late night salivary cortisol level (increased), and low-dose dexamethasone suppression test
1. Low-dose dexamethasone suppresses cortisol in normal individuals but fails to
suppress cortisol in all causes of Cushing syndrome

60
Q

How is plasma ACTH distinguished from ACTH-dependent causes of Cushing syndrome

A

Plasma ACTH distinguishes ACTH-dependent causes of Cushing syndrome from
ACTH-independent causes
1. If ACTH-independent, next step is CT to look for an adrenal lesion. 2. If ACTH-dependent, next step is high-dose dexamethasone test.
E. High-dose dexamethasone suppresses ACTH production by a pituitary adenoma (serum cortisol is lowered) but does not suppress ectopic ACTH production (serum cortisol remains high)

61
Q

How is hypercortisolism treated

A

Treatment generally involves surgical resection
Ketoconazole or metyrapone useful if surgery is not an option

62
Q

What are the effects of 17-hydroxylase deficiency

A

17-hydroxylase deficiency leads to decreased cortisol and androgens
1. Weak mineralocorticoids (DOC) are increased leading to HTN with mild hypokalemia; renin and aldosterone are low
2. Decreased androgens lead to primary amenorrhea and lack of pubic hair (females) or ambiguous genitalia with undescended testes (males)
Newborn screening for CAH via serum 17-hydroxyprogesterone is routine

63
Q

What are the effects of 11-hydroxylase deficiency

A

11-hydroxylase deficiency also leads to androgen excess, but weak mineralocorticoids (DOC) are increased
1. Deoxycorticosterone (DOC) leads to HTN (sodium retention) with mild hypokalemia; renin and aldosterone are low
2. Clitoral enlargement is seen in females

64
Q

Due to enzymatic defects in cortisol production; autosomal recessive
1. High ACTH (decreased negative feedback) leads to bilateral adrenal hyperplasia
2. Mineralocorticoids and androgens may be increased or decreased depending on the enzyme defect.
21-hydroxylase deficiency is the most common cause (90% of cases)
1. Aldosterone and cortisol are decreased; steroidogenesis is shunted towards androgens
2. Classic form presents in neonates as hyponatremia and hyperkalemia with life- threatening hypotension (salt-wasting type); females have clitoral enlargement (genital ambiguity)
3. Nonclassic form presents later in life with androgen excess leading to precocious puberty (males) or hirsutism with menstrual irregularities (females)
What condition could this be

A

CAH

65
Q

Newborn screening for CAH via ……… is routine

A

Serum 17-hydroxyprogesterone
Increased in 21- and 11-hydroxylase deficiency
Decreased in 17-hydroxylase deficiency

66
Q

What is the treatment for CAH

A

Treatment for CAH is glucocorticoids; mineralocorticoids (21-hydroxylase deficiency) or sex steroids (17-hydroxylase deficiency) given as necessary

67
Q

Deficiency of adrenal hormones
Acute insufficiency presents as weakness and shock. Causes include
1. Abrupt withdrawal of glucocorticoids
2. Treatment of Cushing syndrome
3. Waterhouse-Friderichsen syndrome - hemorrhagic necrosis of the adrenal
glands, classically due to sepsis and DIC in young children with
Neisseria meningitidis infection
Chronic insufficiency (Addison disease) presents with vague, progressive symptoms
such as hypotension, weakness, fatigue, nausea, vomiting, and weight loss
What condition could this be

A

Adrenal insufficiency

68
Q

What are some clinical presentations of adrenal insufficiency

A

Weakness
Shock

69
Q

What is Waterhouse-Friderichsen syndrome

A

Hemorrhagic necrosis of the adrenal
glands classically due to sepsis and DIC in young children with
Neisseria meningitidis infection

70
Q

What are some presentations of Addison’s disease

A

Chronic insufficiency (Addison disease) presents with vague, progressive symptoms
such as hypotension, weakness, fatigue, nausea, vomiting, and weight loss

71
Q

What are some common causes for Addison’s disease

A

Autoimmune destruction (most common cause in the West)
TB (most common cause in the developing world)
Metastatic carcinoma (e.g., from lung).

72
Q

May also arise with pituitary (secondary) or hypothalamic (tertiary) disease.
1. Hyperpigmentation (high ACTH) and hyperkalemia (low aldosterone) suggest primary adrenal insufficiency; secondary/tertiary insufficiency has no hyperpigmentation (low ACTH) and normal potassium (normal aldosterone)
2. Lack of ACTH response with metyrapone stimulation test supports a secondary or tertiary cause.
3. ACTH response with CRH stimulation test suggests hypothalamic (tertiary) disease
What condition could this be

A

Addison’s disease

73
Q

What is the treatment for Addison’s disease

A

Glucocorticoids
Mineralocorticoids

74
Q

What is the adrenal medulla composed of

A

Composed of neural crest-derived chromaffin cells
Main physiologic source of catecholamines (epinephrine and norepinephrine)

75
Q

What are some clinical features of pheochromocytoma

A

Clinical features are due to episodic release of catecholamines
Episodic HTN
Headaches
Palpitations
Tachycardia
Sweating

76
Q

How is pheochromocytoma diagnosed

A

Diagnosed by increased metanephrines and catecholamines in serum and urine

77
Q

How is pheochromocytoma treated

A

Treatment is adrenalectomy.
Catecholamines may leak into the bloodstream upon manipulation of the tumor
Phenoxybenzamine (irreversible α-blocker) followed by β-blocker is
administered preoperatively to prevent a hypertensive crisis

78
Q

Tumor of chromaffin cells
Often follows the ‘rule of 10s:’ 10% bilateral, 10% familial, 10% malignant, and 10% located outside of the adrenal medulla (e.g., organ of Zuckerkandl at the inferior mesenteric artery root or bladder wall)
1. Malignancy is defined by metastatic spread; patients require long-term follow-up
Associated with MEN 2A and 2B (RET), von Hippel-Lindau disease, and
neurofibromatosis type 1
What condition could this be

A

Pheochromocytoma

79
Q

What is the treatment for pituitary adenoma

A

Octreotide (somatostatin analog that suppresses GH release)
GH receptor antagonists
Surgery

Pathoma (2 decks)

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