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USMLE Step I Pathology > Endocrine Pathology (Pathoma) > Flashcards

Endocrine Pathology (Pathoma) Flashcards

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USMLE® Step 1 flashcards
1
Q

Pituitary Adenoma

A

Benign tumor of anterior pituitary cells

May be functional or nonfuntional

Nonfunctional present w/ mass effect: bitemporal hemionopsia (compression of optic chiasm), hypopituitarism, and headache

Functional tumors: Present w/ features based on hormone produced (MC is prolactinoma). Also GH adenoma, ACTH adenoma, TSH, LH, and FSH are rare

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2
Q

Prolactinoma

A

MC functional pituitary adenoma

Galactorrhea and amenorrhea (females); decreased libido and headaches (males)

Rx: = dopamine agonists (bromocriptine) or surgery

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3
Q

Growth Hormone Adenoma

A

Gigantism in children

Acromegaly in adults (cardiac failure is MCC of death

Secondary DM is often present

Dx w/ elevated GH and IGF-1

Lack of GH suppression by oral glucose

Rx: Octreotide, GH receptor antagonists, surgery

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4
Q

Hypopituitarism

A

Insufficient productions of hormones by Ant. Pit.

Causes: Pituitary Adenoma (adults –> mass affect or bleeding) or craniopharyngioma (children), Sheehan syndrome, Empty sella syndrome

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5
Q

Sheehan syndrome

A

Pituitary grows great deal during pregnancy, but blood supply doesn’t. –> susceptible to hypoperfusion –> blood loss during pregnancy –> hypopituitarism

Present w/ Poor lactation and loss of pubic hair

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6
Q

Empty Sella Syndrome

A

Sella is empty and pit. is misisng.

Either due to trauma or congenital malformation allowing herniation of arachnoid CSF into sella

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7
Q

Central Diabetes Insipidus

A

ADH deficiency

Due to hypothalamic or posterior pit. pathology (i.e. tumor, trauma, infx)

Polyuria and polydipsia

Hypernatremia and high serum osmolarity

low urine osmolarity and specific gravity

Dx: water deprivation fails to increase urine osmolarity. Responds to desmopressin (vs. nephrogenic).

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8
Q

Nephrogenic Diabetes Insipidus

A

Impaired renal response to ADH

Due to inherited mutations or drugs (lithium or demeclocyline)

Similar to central DI, but there is no response to desmopressin

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9
Q

SIADH

A

Clinical features: hyponatremia and low serum osmolarity –> mental status changes and seizures.

Causes: ectopic production (small cell carcinoma); CNS trauma; pulmonary infection; drugs (cyclophosphamide)

Rx: Free water restriciton, demeclocycline

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10
Q

Thyroglossal Duct Cyst

A

Cystic dilitation of thyroglossal duct (develops from base of tongue and descends) remnant

Presents as anterior neck mass

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11
Q

Lingual thyroid

A

Persistence of thyroid tissue at base of tongue

Presents as base of tongue mass*

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12
Q

Hyperthyroidism

A

Increased level of circulating thyroid hormone

Increases BMR (increases synthesis of Na/K ATPase)

Increases sympathetic nervous system (increase Beta-1 receptors)

Clinical features:

  • Weight loss despite increased appetitite
  • Heat intolerance and sweating
  • Tachycardia w/ increased cardiac output
  • Arrhythmia (esp. A-fib), esp. in elderly
  • Tremor, anxiety, insomnia, and heightened emotions
  • Staring gaze w/ lid lag
  • Diarrhea and malabsorbtion
  • Oligomenorrhea
  • Bone resorption w/ hypercalcemia
  • Decreased muscle mass with weakness
  • *Hypocholesterolemia and Hyperglycemia

MCC = Graves Disease

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13
Q

Graves Disease

A

Autoantibody (IgG) that stimulates TSH receptor –> increased synthesis and release of thyroid hormone

MCC of hyperthyroidism

Occurs in women of childbearing age (like other autoimmune)

Clinical features: Hyperthyroidism, diffuse goiter, and exopthalmos and pretibial myxedema (fibroblasts stimulated by TSH like antibody.

“Scalloped colloid” on histology

Labs: Increased total and free T4; low TSH; Hypocholesteremia and hyperglycemia

Rx: Beta-blockers; Thioamide (blocks peroxidase), and radioiodine ablation.

Thyroid storm is feared complication

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14
Q

Thyroid Storm

A

Feared complication of hyperthyroidism

Elevated catecholamines and massive hormone excess (stress)

Arrhythmia, hyperthermia, and vomiting w/ hypovolemic shock

Treat w/ PTU (inhibits peroxidase and T4–>T3 conversion), Beta blockers, and steroids

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15
Q

Multinodular Goiter

A

Enlarged thyroid gland with multiple nodules

Due to relative iodine deficiency

Usually nontoxic (euthyroid)

Rarely regions become TSH-independent = toxic goiter –> secretes excess T4

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16
Q

Cretinism

A

Hypothyroidism in neonates

Clinical features: Mental retadation, short stature w/ skeletal abnormalities, coarse facial features, enlarged tongue, and umbilical hernia

Causes: Maternal hypothyroidism during early pregnancy, thyroid agenesis, dyshomonogenetic disorder (lack of thyroid peroxidase is MC), or lack of Iodine

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17
Q

Myxedema

A

Hypothryoidism in adults

Clinical features:

  • Myxedema (dough like swelling due to fibroblast proliferation due to high TSH. Esp in larynx = deep voice and tongue)
  • weight gain despite normal appetite
  • Slowing of mental activity
  • Muscle weakness
  • Cold intolerance w/ decreased sweating
  • Bradycardia w/ decreased cardiac output
  • Oligomenorrhea
  • Hypercholesterolemia
  • Constipation

Causes: Iodine deficiency, Hashiomoto’s thyroiditis (MCC), drugs (lithium), or surgical removal/radioablation

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18
Q

Hashiomoto’s Thyroiditis

A

Commonly associated w/ HLA DR5

MCC of hypothyroidism

Autoimmune attack of thyroid gland

Clinical features: Intially can be hyperthyroidism (destruction of cells) and eventually become hypothyroidism –> low T4 and high TSH.

Antithyroglobulin and anti-microsomal antibodies are often present (markers, not mediators)

Histologically: Inflammation w/ formation of germinal centers. Pink cells around germinal centers (Hurtle cells)

Increased risk of B-cell lymphoma

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19
Q

Subacute (deQuervain) Granulomatous thyroiditis

A

Granulomatous thyroiditis that follows a viral infection

Presents as *TENDER thryoid with transient hyperthyroidism

Self-limited; does not progress to hypothyroidism

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20
Q

Reidel Fibrosing Thyroidism

A

Chronic inflammation with extensive fibrosis of thyroid

  • Presents as hypothyroidism with “hard as wood” nontender thyroid gland
  • Fibrosis may extend to local structures (i.e. airway). –> ddx vs. anaplastic carcinoma (young female vs. older patient)
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21
Q

Thyroid Neoplasia

A

Present as distinct, solitary nodule

Thyroid nodules are more likely to be benign than malignant

131 I radioactive uptake studies. Increased uptake seen in Graves or nodular goiter. Decreased uptake seen in adenoma and carcinoma and warrants FNA biopsy*

22
Q

Follicular Adenoma

A

Benign proliferation of follicles surrounded by fibrous capsule

Usually not functional

23
Q

Papillary Carcinoma

A

MC type of thyroid carcinoma (80%)

Exposure to ionizing radiation in childhood is major risk factor.

Histology: Nuclear features (orphan-annie eye and grooves) and possible psammoma bodies are key identifiers.

Often spreads to cervical lymph nodes; rarely metastasizes

Good prognosis (thyroid cancers prevalence and aggressiveness are inverse)

24
Q

Follicular Carcinoma

A

Malignant proliferation of follicles

Surrounded by fibrous capsule with invasion through capsule* (ddx vs. follicular adenoma)

FNA cannot distinguish from follicular carcinoma vs adenoma (can’t see capsule invasion on FNA which is key)

Hematogenous metastasis (backwards carcinoma. Others include renal cell, hepatic, follicular, and choriocarcinoma )

2nd MC tumor. Good prognosis (thyroid cancers prevalence and aggressiveness are inverse)

25
Q

Medullary Carcinoma

A

Malignant proliferation of parafollicular C cells

High levels of calcitonin produced by tumor may lead to hypocalcemia

Calcitonin often deposits within tumor as amyloid. *

Familial cases associated w/ MEN 2A and 2B. Associated w/ RET mutations. Detection of RET mutation warrants prophylactic thyroidectomy.*

26
Q

Anaplastic Carcinoma

A

Undifferentiated malignant tumor of thyroid

Usually seen in elderly (ddx. vs. Ridell’s thyroiditits).

Often invades local structures leading to dysphagia or respiratory compromise

Poor prognosis, but rare

27
Q

Primary Hyperparathyroidism

A

Excess PTH due to disorder of parathyroid gland

Can be from parathyroid adenoma, hyperplasia, or carcinoma. Adenoma is MCC

28
Q

Parathyroid Adenoma

A

Benign neoplasm, usually involving one gland

Usually asx

Features:

  • Nephrolithiasis
  • Nephrocalcinosis
  • CNS disturbances (depression and seizures)
  • Constipation, peptic ulcer disease, and acute pancreatitis* (Ca++ is enzyme activator)
  • Osteitis fibrosis cystica

Lab findings:

  • High PTH
  • High Ca; Low phosphate
  • Increased urinary cAMP (PTH works through Gs on tubular cells)
  • Increased serum Alk Phos (due to activation of Osteoblast stimulation (which bind PTH and then release RANKL –> osteoclasts)

Rx: Surgery

29
Q

Secondary Hyperparathyroidism

A

Excess production of PTH due to disease process extrinsic to parathyroid gland

MCC is CKD (chronic hyperphosphatemia and subsequent low free Ca++ stimulates PTH release)

Lab findings:

  • Increased PTH
  • Low serum Ca++
  • High serum phosphate
  • High Alk Phos
30
Q

Hypoparathyroidism

A

Low PTH

Causes include AI, surgery, and Digeorge

Presents w/ perioral numbness and tingling. Muscle spasms (Chovestk’s sign and Trousseau’s sign), low PTH and low Ca

31
Q

Pseudohypoparathyroidism

A

Due to end-organ resistance to PTH (mutation in Gs)

Hypocalcemia with high PTH

Autosomal dominant form is associated w/ short stature and short 4th and 5th digits.

32
Q

Type I DM

A

Insulin defiency due to AI destruction of B cells

Inflammation of islets

Association w/ DR3 and DR4

Autoantibodies vs. Insulin often present

Presents in childhood w/ features of insulin deficiency:

  • high serum glucose
  • Weight loss, low muscle mass, and polyphagia
  • Polyuria, polydipsia, and glycosuria

Treatment is lifelong insulin

Risk for DKA

33
Q

DKA

A

Excess serum ketoacids

Often arises with stress (infection) –> epi is synergistic w/ glucagon raises blood sugar, exacerbates lipolysis (become ketones)

Clinical features:

  • Hyperglycemia
  • Anion gap acidosis
  • Hyperkalemia (low stores however). Due to lack of insulin which normally drives in K+ and H+/K+ buffering
  • Kussmaul breathing, dehydration, nausea, vomiting, mental status chages, fruity smelling breath

Rx: Fluids, Insulin, Replace electrolytes (K+)

34
Q

Type 2 DM

A

End-organ isulin resistance leading to metabolic disorder characterized by hyperglycemia

MC type of DM; incidence is rising.

Arises in middle-aged, obese adults –> obesity leads to decreased number of insulin receptors

Strong genetic predisposition (higher than DM I)

Insulin levels are high early, low due to exhausion.

Histology reveals amyloid deposition in islets

Clinical features:

  • Polyuria
  • Polydyspsia
  • Often silent

Dx by: Random glucose >200; fasting >126; Glucose tolerance test >200

Rx; Weight loss. Drug therapy, Insulin

Risk for hyperosmolar non-ketotic coma

NEG of vascular BM:

  • Large and medium sized vessels –> atherosclerosis
  • NEG of small vessels leads to hyaline arteriolocslerosis
  • NEG of hemoglobin –> HbA1C

Osmotic damage (esp. cells that take up sugar w/o insulin and w/ aldose reductase)

  • Schwann cells (neuropathy)
  • Pericytes of retinal blood vessels
  • Lens (cataracts)
35
Q

Hyperosmolar non-ketotic coma

A

High glucose levels (>500) leads to life threatening diuresis.

Hypotension and coma

Ketones are absent (some insulin)

36
Q

Pancreatic Endocrine Tumors

A

Tumor of islets cells

Often a component of MEN1 (along w/ parathyroid hyperplasia and pituitary adenoma)

37
Q

Insulinoma

A

Episodic hypoglycemia w/ mental status changes that are relieved by glucose

Low glucose, high insulin and *** high C-peptide

38
Q

Gastrinoma

A

Treatment-resistant peptic ulcers (ZE syndrome)

May be multiple and extend into jejunum

39
Q

Somatistatinoma

A

Achlorhydria (inhibition of gastrin)

Cholelithiasis and steatorrhea (inhibition of CCK)

40
Q

VIPoma

A

Excessive VIP

Water diarrhea, hypokalemia and achlorhydria (WDKA syndrome)

41
Q

Cushing Syndrome

A

Excess cortisol

Sx:

  • Muscle weakness w/ thin extremities
  • Moon facies, buffalo hump, and truncal obesity
  • Abdominal striae
  • HTN (increased alpha-1 receptors)
  • Osteoporosis
  • Immune suppression (1. inhibits phospholipase A2 2.) inhibits IL-2, and 3.) inhibits histamine)

Dx: Increased 24-hr. cortisol syndrome

4 Major causes:

  • Exogenous corticosteroids (bilateral adrenal atorphy)
  • Adrenal probs (Adrenal adenoma, hyperplasia, or carcinoma –> unilateral large adrenals)
  • ACTH-secreting pituitary adenoma (both adrenals big = cushing’s disease)
  • Paraneoplastic ACTH secretion (Both adrenals are big, most commonly due to Small cell lung cancer)

DDX between Cushing’s disease and paraneoplastic is by high-dose dexamethasone suppression test. Ectopic doesn’t suppress.

42
Q

Primary Hyperaldosteronism

A

Principal cell will increase Na resorption in exchange for K+ (hypernatremia and hypokalemia)

Alpha-intercalated cells will dump H+ (Metbaolic alkalosis)

MC due to adrenal adenoma (rarely sporadic hyperplasia or carcinoma)

Characterized by high aldosterone and low renin

43
Q

Secondary Hyperaldosteronism

A

Activation of RAAS due to fibromuscular dysplasia or renal-artery atherosclerosis.

Characterized by high aldosterone and high renin.

44
Q

Congenital Adrenal Hyperplasia

A

Excess sex steroids w/ hyperplasia of both adrenal glands

21-a hydroxylase def. is MCC

All subtypes lack cortisol which results in lack of negative feedback on ACTH resulting in hyperplasia.

45
Q

21-a hydroxylase deficiency

A

MCC of congenital adrenal hyperplasia (continuous ACTH secretion in response to low cortisol)

Inability to convert pregnilone into cortisole or aldo. Excess shunted to sex steroids

Causes clitoral enlargement in females and precocious puberty in males.

Also results in life threatening hypotension and bilateral adrenal enlargement and salt wasting (hyponatremia and hyperkalemia w/ hypovolemia)

46
Q

11-a hydroxylase defiency

A

Same as 21-a hydroxylase def. without salt wasting becasue you are able to make a somewhat active form of mineralocorticoids.

47
Q

17-a hydroxylase deficiency

A

Inability to change pregnilone into cortisol or sex steroid precursors.

Excess mineralocorticoids and lack of sex steroids and cortisol.

48
Q

Adrenal Insufficiency

A

Lack of adrenal hormones

Acute insuffiency may arise w/ Waterhous-Friedrichsen syndrome

Chronic insufficiency is due to progressive destruction of glands

AI destruction (MCC in West), TB (MCC in developing world), or metastatic carcinoma (lung cancer)

Features:

  • Hypotension
  • Hyponatremia, hypovolemia, and hyperkalemia
  • Weakness
  • Hyperpigmentation (Excess ACTH demand –> excess POMC precursor –> also produces Melanocyte Stimulating Hormone
  • Vomiting and diarrhea
49
Q

Waterhouse-Friedrichsen Syndrome

A

Young child w/ Neisseria meningitidis infection w/ DIC leading to hemorrhage in both adrenals –> lack of cortisol –> worsened hypotension

Adrenals that look like a sac of bleed.

50
Q

Pheochromocytoma

A

Tumor of Adrenal Medulla of enterochromaffin cells (brown)

Features:
-Epidsodic hypertension, headaches, palpitations, tachycardia, and sweating

Dx: w/ increased serum metanephrines and increase 24hr. urine metanephrines and VMA

Rx: surgical excision and phenoxybenzamine (alpha-blockers)

10% disease (bilateral, malignant, familial, located outside adrenal medulla, esp. bladder walls).

Associations of MEN2A and 2B. VHL disease. NF type 1.

USMLE Step I Pathology (14 decks)

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