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Pathology > Exam 9 > Flashcards

Exam 9 Flashcards

1
Q

Sheehan Syndrome

A
  • Ischemic necrosis of the pituitary gland leading to hypopituitarism
  • Affects women in postpartum period
    • During pregnancy, pituitary doubles in size but blood supply remains the same
  • Presentation: impaired lactation, loss of pubic hair, fatigue
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2
Q

Rathke Cleft Cyst

A
  • Remnants from embryonic development can accumulate fluid, become cystic, and expand
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3
Q

Empty Sella Syndrome

A
  • Malformation of sella turcica that becomes filled with CSF
  • Pituitary gland is compressed/flattened so that the sella turcica appears flattened
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4
Q

Diabetes Insipidus

A
  • Low ADH secondary to head trauma, surgery, tumors, and inflammatory disorders of the hypothalamus and pituitary
  • Presentation: polyuria, polydipsia, increased serum sodium, low spec. gravity of urine
  • Dx: Water deprivation test
  • Tx: Desmopressin
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5
Q

Syndrome of Inappropriate ADH (SIADH)

A
  • High ADH causing resorption of excessive amounts of free water, leading to hyponatremia
  • Presentation: hyponatremia, low serum osmolarity, cerebral edema, neurologic dysfunction/seizures
  • Tx: water retention, demeclocycline
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6
Q

Craniopharyngioma

A
  • Derived from remnants of Rathke’s pouch
  • Rare, benign, bimodal distribution (children & elderly)
  • Presentation: growth retardation (children), headaches and visual disturbances (elderly)
  • Two histological variants
    • Adamantinomatous craniopharyngioma (children)
    • Papillary craniopharyngioma (elderly)
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7
Q

Pituitary Carcinoma

A
  • Malignant counterpart of pituitary adenoma
  • Very rare
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8
Q

Congenital Malformations of the Thyroid Gland

A
  • Thyroglossal Duct Cyst
  • Lingual Thyroid
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9
Q

Hyperthyroidism

A
  • Elevated T3 and T4 results in a hypermetabolic state
  • Increases basic metabolic rate and sympathetic nervous system activity
  • Clinical features
    • Weight loss, heat intolerance, arrythmias, anxiety, insomnia, oligomenorrhea
    • Ocular changes: lid lag
    • GI hypermobility, malabsorption
    • Osteoporosis
  • High levels of T3/4, low levels of TSH
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10
Q

Thyroid Storm

A
  • Acute, life-threatening, hypermetabolic state caused by abrupt onset of severe hyperthyroidism
  • Most common in patients with Graves Disease
  • Clinical Presentation: fever, tachycardia, HTN, GI symptoms
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11
Q

Renal Papillary Adenoma

A
  • Benign
  • Found in the renal cortex
  • Arise from renal tubular epithelium
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12
Q

Oncocytoma

A
  • Benign
  • Arise from intercalated cells of collecting ducts
  • Mahogany brown color
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13
Q

Angiomyolipoma

A
  • Benign
  • Associated with tuberous sclerosis
    • Lesions of cerebral cortex, epilepsy, mental retardation, SEGA, angiofibromas, rhabdomyomas
  • Can bleed spontaneously
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14
Q

Renal Cell Carcinoma

A
  • Most common renal malignant tumor
  • 6th-7th decade; M>F; tobacco use
  • Only 4% are familial variants
    • Von Hippel-Lindau Syndrome
    • Hereditary Clear Cell Carcinoma
    • Hereditary Papillary Carcinoma
  • Frequently invades renal veins or the vena cava
  • Most often arises at the renal poles
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15
Q

Clear Cell Carcinoma

A
  • Histological variant of RCC
  • Most common type
  • Majority are sporadic
  • Majority are associated with loss of sequences on short arm of chromosome 3
  • Grading (Fuhrman) based on nuclear size and presence of nucleoli
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16
Q

Papillary Carcinoma

A
  • Histological variant of RCC
  • Characterized by papillary growth pattern
  • Frequently multifocal and bilateral
  • Associated with Dialysis-associated Cystic Disease
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17
Q

Chromophobe Renal Carcinoma

A
  • Histological variant of RCC
  • Prominent cell borders with eosinophilic cytoplasm
  • Excellent prognosis
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18
Q

Collecting Duct (Bellini Duct) Carcinoma

A
  • Histological variant of RCC
  • Rarest of the four
  • Arise from collecting duct cells in the medulla
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19
Q

What are the clinical features of renal cell carcinoma?

A
  • Three classical features (seen in 10%):
    • Costovertebral pain
    • Palpable mass
    • Hematuria (most reliable)
  • Other symptoms: fever, malaise, weakness, weight loss
  • Paraneoplastic syndromes: polycythemia, hypercalcemia, htn, hepatic dysfunction, Cushing syndrome, etc.
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20
Q

What are the most common locations of metastasis in renal cell carcinoma?

A
  • Lungs (>50%)
  • Bones (33%)
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21
Q

Urothelial Carcinomas of Renal Pelvis

A
  • Become rapidly clinically apparent, producing hematuria (due to fragmentation of tumor)
  • Associated with pre-existing bladder tumor and analgesic nephropathy
  • Benign Papilloma or Invasive Urothelial Carcinoma
  • More often malignant than benign
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22
Q

What are the two precursor lesions to Invasive Urothelial Carcinoma?

A
  • Papillary lesions can lead to:
    • Papillomas (benign; <1%)
    • Inverted Papillomas (benign; inter-anastomosing cords of urothelium extending toward the lamina propria)
    • Low-grade Papillary Urothelial Carcinoma
    • High-grade Papillary Urothelial Carcinoma (higher incidence of invasion into muscular layer)
  • Flat lesions can lead to:
    • Carcinoma In-Situ/Flat Urothelial Carcinoma (pagetoid spread)
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23
Q

Squamous Cell Carcinoma

A
  • Bladder carcinoma associated with schistosomiasis
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24
Q

Adenocarcinoma

A
  • Bladder carcinoma
  • Arise from urachal (embryonic) remnants or in association with intestinal metaplasia
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25
Q

What is the most common mesenchymal tumor overall and most common sarcoma in adults?

A
  • Leiomyoma (most common overall)
  • Leiomyosarcoma (most common sarcoma in adults)
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26
Q

Peyronie Disease

A
  • Fibrous bands involving corpus cavernosum of penis
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27
Q

What are the characteristics of Nephrotic Syndrome?

A
  • Urinary loss of plasma proteins (proteinuria, >4g/day)
  • Increased basement membrane permeability
  • Hypoalbuminemia –> edema
  • Hyperlipidemia and Hypercholesterolemia
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28
Q

Minimal Change Disease

A
  • Most common in children
  • Fusing of foot processes on EM
  • Good response to steroids
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29
Q

Focal Segmental Glomerulosclerosis

A
  • Pts somewhat older compared to MCD
  • Usually resistant to steroid therapy
  • Juxtamedullary glomeruli demonstrate sclerosis within capillary tufts
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30
Q

Membranous Glomerulonephritis (Membranous Nephropathy)

A
  • Highest incidence in teenagers and young adults
  • Marked thickening of basement membrane
  • Numerous electron-dense immune complexes
    • “Spike and dome” appearance
  • Poor response to steroids
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31
Q

Diabetic Nephropathy

A
  • Increased thickness of glomerular basement membrane
  • Thickened and sclerosed afferent and efferent arterioles
  • Increase in mesangial matrix causing:
    • Diffuse Glomerulosclerosis
    • Nodular Glomerulosclerosis (Kimmelstiel-Wilson Nodules)
  • Armanni-Ebstein Lesion: accumulation of glycogen in tubular cells in long-standing hyperglycemia
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32
Q

Amyloidosis

A
  • Primarily subendothelial and mesangial deposits
  • Identified by congo red stain and apple-green birefringence under polarized light
  • Characteristic criss-cross fibrillary pattern of amyloid
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33
Q

Lupus Nephropathy

A
  • Renal component of SLE
  • 5 Classes
    • Class IV (Diffuse Proliferative Glomerulonephritis)
      • Most common, most severe
  • Subendothelial immune complex deposition
  • “Wire loop” abnormality
  • “Fingerprint” pattern
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34
Q

What are the characteristics of Nephritic Syndrome?

A
  • Glomerular inflammation and bleeding into urinary space
  • Oliguria
  • Azotemia
  • Hypertension
  • Hematuria with RBC casts
  • Limited proteinuria
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35
Q

Acute Proliferative (Poststreptococcal) Glomerulonephritis

A
  • Majority associated with streptococcal (group A) infection
  • Subepithelial immune complex disease
  • Large, hypercellular, bloodless glomeruli
  • Subepithelial electron-dense “humps”
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36
Q

Rapidly Progressive (Crescentic) Glomerulonephritis

A
  • Characteristic crescent formation from proliferation of parietal cells of Bowman’s capsule
  • Rapidly progresses to renal failure within weeks to months
  • Can be caused by Goodpasture Syndrome
    • Antiglomerular besement membrane antibodies
    • Linear immunofluorescence
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37
Q

Alport Syndrome

A
  • Hereditary nephritis associated with nerve deafness and ocular disorders
  • Defect in Type IV collagen
  • Thinning and splitting of the glomerular basement membrane
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38
Q

IgA Nephropathy (Berger Disease)

A
  • Characteristic IgA deposition in the mesangium
  • Associated with Henoch-Schonlein Purpura
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39
Q

Membranoproliferative Glomerulonephritis

A
  • Characterized by basement membrane thickening and cellular proliferation
  • Reduplication of glomerular basement membrane into two layers creating “tram-track”** appearance**
  • Two forms:
    • Type I: immune complex nephritis; striking “tram-track” appearance
    • Type II: “tram-track” appearance less apparent; dense-deposits within glomerular basement membrane
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40
Q

Urinary Tract Obstruction

A
  • Increases susceptibility to infection and stone formation
  • Clinical features:
    • Hydronephrosis
    • Renal colic
    • Pain
    • Oliguria, Anuria
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41
Q

Urolithiasis

A
  • Most arise in renal pelvis and calyces
  • Form due to supersaturation of urine
42
Q

Calcium Oxalate Stones

A
  • Most common type
  • Arise due to hypercalcemia and hypercalciuria
  • Mechanism: nucleation of calcium oxalate by uric acid crystals in the collecting duct
43
Q

Magnesium Ammonium Phosphate Stones

A
  • Due to infections by bacteria
  • Staghorn calculi
44
Q

Uric Acid Stones

A
  • Common in gout and leukemia
  • Only stones that are radiolucent
45
Q

Cystine Stones

A
  • Least common of the four
  • Caused by genetic defects in the renal reabsorption of cystine leading to cystinuria
  • Form at low urinary pH
46
Q

What are the clinical symptoms of urinary tract stones?

A
  • Severe, intermittent flank pain often radiating to the groin
  • Nausea, vomiting, hematuria
  • Costovertebral angle tenderness
47
Q

Acute Pyelonephritis

A
  • E. Coli is most common cause
  • Clinical Presentation:
    • Fever, flank pain, dysuria, urgency
  • Findings: WBC casts in urine, increased WBCs, findings of cystitis
48
Q

Renal Papillary Necrosis

A
  • Associated with DM (most common), Analgesic abuse (phenacetin), Sickle cell disease
  • Ischemia due to marginal blood supply of medulla
  • Clinical presentation:
    • Bilateral and diffuse: ARF, fever, chills, flank pain, hematuria
    • Insidious: concentrating defect or progressive renal failure
49
Q

Xanthogranulomatous Pyelonephritis

A
  • Destructive chronic histiocytic inflammation
  • Clinical presentation:
    • Renal mass, pain, fever
50
Q

Chronic Pyelonephritis

A
  • Chronic tubulointerstitial inflammation
  • “Thyroidization” of kidney–atrophic tubules that look like thyroid follicles
51
Q

Cystitis

A
  • Clinical presentation:
    • Dysuria, increased urinary frequency, urgency, suprapubic pain
  • Cloudy urine, >10WBC/HPF, + Leukocyte esterase, + Nitrites, >100k CFU
52
Q

Urethritis

A
  • Causes: E. Coli, Chlamydia, Neisserria
  • Clinical presentation:
    • Dysuria, urgency of urination
  • Negative urine culture, >10WBC/HPF
53
Q

AD (Adult) Polycystic Kidney Disease

A
  • Multiple expanding cysts of both kidneys
  • Mutation in genes on chromosome 16p13.3 (PKD1) and 4q21 (PKD2)
    • PKD1: 85% of cases; more severe; localized to tubular epithelial cells of distal nephron
    • PKD2: 15% of cases; less severe; localized to all segments of renal tubules
  • Clinical features:
    • Renal insufficiency, pain, renal colic, heamturia, proteinuria, polyuria, htn
    • Polycystic liver disease (40%), Berry aneurysms, mitral valve prolapse
54
Q

AR (Childhood) Polycystic Kidney Disease

A
  • Mutation of PKHD1 gene of chromsome 6p21-p23
  • Develop congenital hepatic fibrosis
55
Q

Medullary Sponge Disease

A
  • Lesions consisting of multiple cystic dilations of the collecting ducts in the medulla
  • Renal function is usually normal
56
Q

Medullary Cystic Disease

A
  • Cysts most prominent at corticomedullary junction
  • Widespread cortical atrophy
  • Glomerular structure is preserved
57
Q

Multicystic Renal Dysplasia

A
  • Abnormality in metanephric differentiation
  • Abnormal kidney architecture, persistence in kidney of abnormal structures (e.g. cartilage), undifferentiated mesenchyme, immature collecting ducts
58
Q

Acquired (Dialysis-associated) Cystic Disease

A
  • Seen in kidneys that have undergone prolonged dialysis
  • Cortical and medullary cysts
  • Cysts often contain calcium oxalate crystals
59
Q

Pituitary Adenomas

A
  • Benign tumors of anterior pituitary
  • Most common cause of hyperpituitarism
  • May secrete one, multiple, or no hormones
60
Q

Prolactinoma

A
  • Most common type of functioning adenoma
  • Clinical features:
    • Amenorrhea & galactorrhea (females)
    • Loss of libido & headaches (males)
  • Tx: Bromocriptine (dopamine agonist)
61
Q

Somatotrophic Adenoma

A
  • Secrete GH
  • Second most common type of adenoma
  • Clinical features:
    • Gigantism (children): linear bone growth, increased height with long arms and legs
    • Acromegaly (adults): enlarged bones of hands, feet, forehead, jaws, tongue, and viscera
62
Q

Corticothophic (ACTH) Adenoma

A
  • Adenoma producing POMC (precuror of ACTH and beta-lipotropin)
  • Excess ACTH –> hypercortisolism
    • Cushing Syndrome
    • Cushing Disease
63
Q

Gonadotrophic Adenoma

A
  • LH and FSH producing adenomas
64
Q

Thyrotroph Adenoma

A
  • TSH producing adenoma
65
Q

Non-functioning Adenomas

A
  • 30% of pituitary adenomas
  • Presentation related to mass effect:
    • Hypopituitarism
    • Bitemporal hemianopsia
    • Headaches
    • Pituitary apoplexy
66
Q

Pituitary Apoplexy

A
  • Hemorrhagic destruction leading to hypopituitarism
  • Excruciating headaches, diplopia, CV collapse
67
Q

Graves Disease

A
  • Most common cause of hyperthyroidism
  • IgG autoantibodies bind to TSH receptor stimulating hormone production
  • F>M; 20-40s
  • Clinical features:
    • Hyperthyroidism
    • Diffuse goiter
    • Exopthalmos and pretibial myxedema
  • Histology: scalloped borders
68
Q

Hypothyroidism

A
  • F>M
  • Manifestations:
    • Cretinism: impaired neural and skeletal development in infancy
    • Myxedema: hypothyroidism that develops in older children or adults, resulting in slowed physical and mental activity; goiter (due to increased TSH)
  • Decreased T3/4, increased TSH
69
Q

What is the most common cause of hypothyroidism worldwide?

A
  • Iodine Deficiency
70
Q

Hashimoto Thyroiditis

A
  • Most common cause of hypothyroidism in iodine-sufficient areas
  • Autoimmune disorder causing gradual destruction of thyroid gland though auto-antibodies
  • F>M; 40-50s
  • Histology: Hurthle cells
71
Q

Subacute (Granulomatous) Thyroiditis (De Quervain Thyroiditis)

A
  • Follows viral infection (Coxsaxkievirus, Mumps, Measles, Adenovirus)
  • F>M; 40-50s
  • Clinical presentation:
    • Painful gland, transient hyperthyroidism
72
Q

Reidel Fibrosing Thyroiditis

A
  • Chronic inflammation and extensive fibrosis
  • Clinical presentation:
    • Hypothyroidism, “hard as wood” painless thyroid
73
Q

Follicular Adenoma

A
  • Benign proliferation surrounded by fibrous cap
  • Unilateral, painless nodule
74
Q

Papillary Carcinoma

A
  • Most common form of thyroid cancer
  • F>M; 20-40s
  • Genetic alterations
    • RET/PTC
    • BRAF
  • Morphology: “Orphan Annie eye” nuclei
75
Q

Follicular Carcinoma

A
  • F>M; 40-60s
  • Invasion through the gland’s fibrous cap
76
Q

Anaplastic (Undifferentiated) Carcinoma

A
  • Rare; elderly
  • Histology: Anaplasia, pleomorphism, variable architecture
  • Clinical presentation:
    • Dyspnea, dysphagia, hoarsness, cough
    • Fixed, rapidly enlarging neck mass
  • Very aggressive with near 100% mortality rate
77
Q

Medullary Thyroid Carcinoma

A
  • Derived from parafollicular C cells
  • Secretes calcitonin
  • Histology: amyloid stromal background
78
Q

Primary Hyperparathyroidism

A
  • Clinical presentation:
    • “Painful bones, renal stones, abdominal groans, psychic moans”
    • Due to high PTH and Ca++
  • F>M
  • Lab: High PTH, High Ca++, Low PO4
79
Q

Parathyroid Adenoma

A
  • Most common cause of primary hyperparathyroidism
  • Solitary
  • Composed of uniform, polygonal chief cells and involve a single gland
80
Q

Secondary Hyperparathyroidism

A
  • Caused by chronic hypocalcemia (of any etiology) resulting in compensatory overactivity of parathyroid gland
  • Most common cause is renal failure
  • Lab: High PTH, Low Ca++, High PO4
81
Q

Di George’s Syndrome

A
  • Caused by deletion of 22q11
  • CATCH-22
    • Cardiac abnormalities (tetralogy of Fallot)
    • Abnormal facies
    • Thymic aplasia
    • Cleft palate
    • Hypocalcemia/Hypoparathyroidism (aplasia)
82
Q

What is Chvostek sign?

A
  • Tapping along facial nerve induces contractions of eye, mouth, or nose muscles
  • Indicates tetany due to hypocalcemia
83
Q

What is Trousseau sign?

A
  • Carpal spasms elicited by filling of a blood pressure cuff
  • Indication of tetany due to hypocalcemia
84
Q

Pseudohypoparathyroidism

A
  • End-organ resistance to PTH
85
Q

Insulinoma

A
  • Most common endocrine neoplasm (most pancreatic neoplasms are exocrine!)
  • Clinical features:
    • Hypoglycemic episodes causing confusion, stupor, loss of consciousness
    • Whipple’s Triad: hypoglycemia, CNS symptoms, reversal by glucose administration
  • Increased C-peptide
86
Q

Gastrinoma

A
  • Hypersecretion of gastrin
  • Arise anywhere within the “Gastrinoma Triangle”
  • Zollinger-Ellison Syndrome
    • Hypergastrinemia
    • Hypersecretion of gastric acid
    • Severe peptic ulceration
    • Diarrhea
87
Q

Glucagonomas

A
  • Clinical features:
    • Mild hyperglycemia
    • Necrolytic migratory erythema
    • Anemia
88
Q

VIPomas

A
  • Secrete vasoactive intestinal peptide (VIP)
  • Clinical features:
    • Watery diarrhea, hypokalemia, achlorhydria (low or absent gastric acid production)
89
Q

Wermer Syndrome

A
  • MEN Type I
  • Affects 3Ps
    • Parathyroid: primary hyperparathyroidism
    • Pancreas: gastrinomas and insulinomas most common
    • Pituitary: prolactin and GH adenomas most common
  • Germline mutation in MEN1 tumor suppressor gene, which affects it’s product Menin
90
Q

Sipple Syndrome

A
  • MEN Type IIa
  • Medullary carcinomas (100%), Pheochromocytoma (50%), Parathyroid hyperplasia (20%)
  • Germline mutation in RET proto-oncogene
  • Loss of function mutation results in Hirschsprung Disease
91
Q

Familial Medullary Thyroid Cancer

A
  • Variant of MEN Type IIa
92
Q

MEN Type IIb

A
  • Medullary thyroid carcinoma: multiple, aggressive, leading cause of death
  • Pheochromocytoma
  • Neuromas/Ganglioneuromas
  • Marfanoid Habitus
93
Q

Cushing Syndrome

A
  • Hypercorticism regardless of cause
  • Most common cause is exogenous adrenal corticoids
94
Q

Cushing Disease

A
  • Adrenal hypercorticism secondary to pituitary disease
  • e.g. corticotropic adenoma –> hypersecretion of ACTH –> increased production of cortical hormones
95
Q

Dexamethasone Suppression Test

A
  • Given at low and high doses
  • Low dose: suppresses cortisol when no pathology in endogenous cortisol production
  • High dose: exerts negative retro-control on pituitary ACTH producing cells, but not on ectopic ACTH producing cells or adrenal adenoma
96
Q

Conn Syndrome

A
  • Primary Aldosteronism
  • Most common cause is adrenocortical adenoma
  • Clinical features:
    • HTN, Na+ and water retention, hypokalemia, decreased serum renin
97
Q

Secondary Aldosteronism

A
  • Secondary to renal ischemia, renal tumors, and profound edema
  • Increased serum renin
98
Q

Adrenal Virilism (Adrenogenital Syndrome)

A
  • Congenital enzyme defect leading to diminished cortisol production
  • Causes:
    • 21-Hydroxylase Deficiency: most common; salt loss and hypotension
    • 11-Hydroxylase Deficiency: salt retention and hypertension
  • Clinical features:
    • Virilism (females), precocious puberty (males)
99
Q

Addison Disease

A
  • Primary Adrenocortical Deficiency (hypocorticism)
  • **Most common **cause is idiopathic adrenal atrophy
  • Clinical features:
    • Hypotension, hyperpigmentation, decreased Na+, Cl-, glucose, bicarb, increased K+
100
Q

Waterhouse-Friderichsen Syndrome

A
  • Catastrophic adrenal insufficiency and vascular collapse
  • Due to hemorrhagic necrosis of adrenal cortex
    • Associated with DIC
    • Classically due to meningococcemia
101
Q

Pheochromocytoma

A
  • Derived from chromaffin cells of adrenal medulla
  • Paroxysmal HTN due to hyperproduction of catecholamines
102
Q

Neuroblastoma

A
  • Highly malignant “small blue cell” catecholamine-producing tumor
  • Occurs in early childhood
  • Causes HTN
  • Amplification of N-myc oncogene

Pathology (3 decks)

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