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Errata/Additions RR3 Pathology: Students

Page 6
3. b. In the medulla, the Na+-K+-Cl- symporter.

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Table 1-2
Bilirubin Kernicterus (see Fig. 15-5): fat-soluble (free unbound) unconjugated.

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Table 2-1: Under Leukotrienes: Montelukast leukotriene receptor antagonist: activity of LTC4,
LTD4, LTE4
Under IL-1, TNF and Functions: TNF is a promoter of apoptosis (refer to Chapter 1)
TNF important in formation/maintenance of granulomas

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5. d. (3) AIDS-defining malignancies
Kaposis sarcoma.primary CNS lymphoma (EBV), cervical carcinoma

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Figure 3-5 C5 convertase is correctly represented as C4b2a3b.

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I. A. 1. c. Potassium (K+ ) is the major intracellular fluid (ICF) cation.
Phosphate (PO42-) major anion.

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Box 4-1
Last paragraph: ATII has a fourfold

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Box 4-1: top of page
1. Vasoconstriction of.
2. Stimulation of
3. Direct stimulation of
4. Enhances activity of H+/Na+ cotransporter in the proximal renal tubule

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A low peritubular capillary hydrostatic pressure (PH) coupled with a high oncotic pressure (PO) is
responsible for enhancing the reabsorption of solutes from the tubular lumen into the tubular cell
out into the lateral intercellular space, and into the peritubular capillary (B). This occurs when
the EABV is decreased (e.g., ECF volume depletion, or hypovolemia). A high PH coupled with a
low PO results in the loss of solutes in the urine in conditions when the EABV is increased (A;
e.g., ECF volume overload, or hypervolemia).
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MN: EABV FF PO > PH
MN: EABV FF PH > PO

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Fig. 4-6. Change cotransporter to symporter

Fig. 4-7 Na+-C- symporter in the early

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Figure 4-6: Sodium, potassium, chloride symporter in the medullary segment of the thick
ascending limb. See text for description (From Goljan EF, Sloka KI: Rapid Review Laboratory
Testing in Clinical Medicine, Mosby Elsevier, 2008, p 34, Fig. 2-6).

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2. Thick ascending limb (TAL medullary segment)
b. Generation of fH2O primarily occurs in the active Na+-K+-2 Cl- symporter (Fig.
4-6)
c. Water proximal to the symporter is obligated (o).
MN: Na+-K+-2Cl- symporter: generates free water
d. Symporter separates oH2O from Na+, K+, and Cl-.
g. Ca2+ is also reabsorbed by the symporter.
h. Cl- binding site in Na+-K+-2 Cl- symporter is inhibited by loop diuretics.
MN: Cl- binding site in Na+-K+-2Cl- symporter: inhibited by loop diuretics

Shaded area discussing loop diuretics


Change both cotransporters to symporter

3. Na+-Cl- symporter
d. Thiazides inhibit the Cl- site in the Na+-Cl- symporter
MN: Thiazides: inhibit Cl- site in Na+-Cl- symporter

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F. Potassium K+ disorders

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Table 4-9 under the Loop and thiazide discussion (2nd from the bottom under Discussion)-
(hypernatremia) should be changed to (hyponatremia).

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B. 1. a. Unequal separation of chromosomes in meiosis

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Table 5-4
Isotretinoin Hearing defectsmental retardation, CNS/cardiovascular defects
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Table 6-1
Hematologic Increased risk for acute myeloblastic leukemia

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Margin note: Oral contraceptives: most common cause of hypertension in young women;
angiotensinogen

Page 115
C. 2. c. (2) Leptin secretion increases when adipose stores are increased
(a) Decreases food intake (via hypothalamus)
(b) Increases energy expenditure (e.g., -oxidation of fatty acids)
(3) Leptin secretion decreases when adipose stores are decreased
(a) Increases food intake (via hypothalamus)
(b) Decreases energy expenditure (e.g., -oxidation of fatty acids)

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B. 4. a. Renal failure (most common cause)

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Margin note: 2nd one down in column: Epithelial,

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C. Nuclear features
1. Benign tumors
a.
b.
2. Malignant tumors
a. Nuclear/cytoplasmic ratio is increased, and nucleoli are prominent
b. Mitoses have normal and atypical mitotic spindles

MN: Loss of intercellular adherence cell invasion

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3. Gynecologic cancer-related deaths (in descending order)
a. Ovary
b. Endometrium
c. Cervix
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Margin Note: Enzymes involved in dimer excision: endonuclease, exonuclease, polymerase,
ligase

Fig. 8-4. Under 4 53 synthesis of a new strand takes place (polymerase), the correct..

Table 8-5
Polycyclic hydrocarbons Adenocarcinoma: distal esophagus, pancreas, kidney

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C. 1. b. (1) Acute myeloblastic or chronic myelogenous leukemia

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C. 1. b. (1) Chronic high levels of tumor necrosis factor- (called cachectin)
Margin note: Hemostasis in malignancy: thrombogenic
Margin note: Signs of ectopic hormone production: hypercalcemia, hyponatremia,
hypoglycemia, hypercortisolism, polycythemia

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a. Acquired causes of hypertriglyceridemia
(1) Diabetes mellitus
Decreased muscle and adipose CPL (enzyme induced by insulin)

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IV.Venous System Disorders


A. Saphenous venous system
1. Superficial veins drain blood into the deep veins via perforating branches.

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(1) Stasis dermatitis
(a) Orange discoloration.
(b) Caused by rupture of perforating branches

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Sturge-Weber syndrome Nevus flammeus (birthmark) on the face in distribution of
(Fig. 9-9D) cranial nerve V (trigeminal)

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Systolic dysfunction is characterized by a low ejection fraction (EF) ( 40%). The EF equals
the stroke volume divided by the left ventricular end-diastolic volume. The normal value ranges
from 55% to 80%. Diastolic dysfunction is characterized by normal to high (delete) EF (stiff
ventricle) and an S4 atrial gallop due to increased resistance to filling in late diastole. There is
an increase in left atrial pressure and pulmonary congestion. If left ventricular filling is
significantly impaired, cardiac output is decreased.

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Margin note: LHF: most common cause RHF

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f. (2) (c) Reversal of blood flow.

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3.c. Iron deficiency
(1) Most common microcytic anemia with an increased RDW

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Margin note: PNH: intrinsic defect, intravascular hemolysis

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MN: Nodal enlargement: <30.

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(6) Epitrochlear
Cat-scratch disease, non-Hodgkins lymphoma (NHL)
(7) Hilar
(a) Metastatic lung cancer
(b) Sarcoidosis (bilateral)

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MN: last one on page correct spelling Hashimotos

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MN: top one on page Histiocytes: CD1 +; contain Birbeck granules

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F. 2. d. Thrombin converts fibrinogen holding platelets together to fibrin at the end of the platelet
phase

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Margin note: Circulating anticoagulant: PT and/or PTT.
F. 3. b. (2) No correction of PT and/or PTT
3. b. (3) Correction of PT and/or PTT

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Margin Note: Normal FEV1sec/FVC: 4/5 L = 80%

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Margin note at top: OSA: excessive snoring with
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Margin note at top: ARDS risk:.

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Margin note at top: Bronchopneumonia: acute bronchitis with local extension into parenchyma

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Table 16-4
Under Klebsiella pneumoniae: under Discussion should be:
Typical pneumonia associated with blood-tinged, thick, mucoid sputum

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Margin note on top: Diagnosis: V/Q scan + spiral CT

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Third Margin note from top
Particle size 1-5 m: bifurcation respiratory bronchioles and alveolar ducts
Particle size < 0.5 m: alveoli

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MN: third one from top: Pre-AIDS lesions: thrush, hairy leukoplakia, aphthous ulcers

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Table 17-1: under Hairy leukoplakia and Features column: Pre-AIDS lesion (refer to Chapter 3)

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Table 17-1: under Congenital syphilis and Features column: Abnormalities involving incisors
(notched and tapered like a peg).

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Margin Note 2nd from the bottom: ZE syndrome: gastrin, acid

Page 338
7. Tests to evaluate pancreatic insufficiency
a. Serum immunoreactive trypsin
(1).
(2) Decreased concentration in chronic pancreatitis
(3) Increased concentration in early cystic fibrosis
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Margin Note 3rd from the top: Serum immunoreactive trypsin: in chronic pancreatitis

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Margin Note 3rd from the top: Celiac disease: anti-tTG, EMA, gliadin antibodies

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Margin Note 2nd from the top: Colon cancer: 3rd most common cause of mortality due to cancer
Margin Note bottom: FOBT: most tests do not distinguish hemoglobin from myoglobin

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Margin note 3rd from the top: Anal fissure: most are posteriorly located; anal tag marks location

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Table 18-1: First row of the table should be CB <20% not UCB <20%

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Box 18-1 First sentence. In viral hepatitis, ALT is higher

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Table 18-5
Under Healthy carrier (2nd row from bottom): under column for Anti-HBc-IgM, it should be
not +
HBsAg HBeAg HBV DNA Anti-HBc-IgM Anti-HBc-IgG Anti-HBs Interpretation
+ + Healthy
carrier

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Delete Margin note (redundant): Alcoholic hepatitis: acetaldehyde damages hepatocytes

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2. c. (2) Mesocaval shunt
Connects the superior mesenteric vein with the vena cava

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First Margin Note
Wilsons disease: total serum copper; serum/urine free copper

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First Margin Note at top: Bile: ..bicarbonate
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Margin note 6th from top: Stage 2: stone..right scapula/shoulder

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4. c. (2) Excellent newborn screen for cystic fibrosis (increased)

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C. 4. b. Decreased serum immunoreactive trypsin

Page 393, Figure 19-1: New schematic. Copy and paste into book.

Page 394
Margin note at top of page: MN: Nephrotoxic drugs in elderly: must adjust
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Table 19-8

Focal segmental glomerulosclerosis Primary or secondary disease; secondary causes HIV


(most common glomerular disease; mainly in young
black males) and intravenous heroin abuse.
Most common cause of nephrotic syndrome in adults
Negative IF; ..
Nonselective
Hypertension
Poor prognosis
Treatment
Diffuse membranous Second most common cause of nephrotic syndrome in
glomerulopathy (see Fig. 19-7) adults
All other material is okay

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H. 1. Alports syndrome
a. X-linked recessive (most common); autosomal recessive/dominant types
Mutations in -chains (3, 4, or 5) of type IV collagen in GBM

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Margin note at top of page: Embryonal rhabdomyosarcoma: most common.

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Margin note 2nd from the bottom: Testicular cancer metastasis: para-aortic

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Margin note 4th from the bottom: Testosterone: synthesized in ovary and adrenals

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Margin note 3rd from the top: Pregnancy respiratory alkalosis due to estrogen/progesterone stimulation of
respiratory center

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E. 1. d. (4) Ovum 46, XX (90% of cases)
(a) Ovum lacks maternal chromosomes
(b) Chromosomes derived from father; duplication of 23X sperm in ovum

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E. 1. e. (2) Normal embryo is present (no chromosome abnormality)
(a) Ovum triploid (69 XXY in 70% of cases; XXX in 27% of cases)
(b) Fertilization 23X ovum by two haploid sperm or one diploid sperm
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Replace all margin note and text 131I with 123I (should be a total of 7 replacements)

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Replace all margin note and text 131I with 123I (should be a total of 2 replacements)

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Replace text 131I with 123I (should be only 1 replacement)

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Replace all margin note and text 131I with 123I (should be a total of 3 replacements)
Note: 8. c. Ablative 131I. is okay; leave as is.

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Table 22-2
Replace table heading (top row) 131I with 123I

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Margin note 3rd from top: PTH feedback: hypocalcemia/hyperphosphatemia PTH;
hypercalcemia/hypophosphatemia PTH

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Table 22-4
Thiazides Mechanism: increases early distal tubule reabsorption of calcium; always consider a
possible underlying parathyroid adenoma (order serum intact PTH)

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3.d. Decreased serum 1,25-(OH)2D
Hypercalcemia decreases synthesis of 1-hydroxylase in proximal renal tubule

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F. 4. b. Hyperphosphatemia inhibits 1--hydroxylase
Table 22-5
Hypovitaminosis D (extrarenal Decreased reabsorption of phosphorus from the
causes) small intestine (remove and kidney)

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Margin note 2nd from top: Peripheral tissue sites to produce DHT: skin..
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Table 22-7

Disorder Serum calcium Serum Serum PTH Serum 25- Serum 1,25-
phosphorus (OH)D OH)2D
Primary HPTH N

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Table 22-10: under somatostatinoma, change to -islet cells.

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Margin note last one at bottom: DKA electrolytes: serum sodium (dilutional)..

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Margin note 3rd from bottom: Alkaptonuria: homogentisic acid

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6. c. Cevimeline (cholinergic agent with muscarinic agonist activity)

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Table 23-3
DeQuervains tenosynovitis Pain on the radial aspect of the wrist aggravated by moving the
thumb

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Table 23-3
Knee joint injuries Unhappy triad: most common internal
(Fig. 23-23C) derangement of knee joint. Valgus injury.
Damage to medial meniscus, medial
collateral ligament, anterior cruciate
ligament; lateral meniscus also commonly
injured
Treatment: physical therapy; arthroscopic
surgery

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Margin note last one on bottom: Eczema: acute eczema weeping; chronic eczema dry

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Margin note 2nd from top: Key findings: seizures, mental retardation, angiofibromas, ash leaf lesions
Page 582
Alignment problem in Table 25-2; move Meningitis and encephalitis to Disease column
Lymphocytic Meningitis and This column is okay
choriomeningitis encephalitis

Page 582 (Copy and paste into book)


TABLE 25-3 SLOW VIRUSES AND SPONGIFORM ENCEPHALOPATHY OF THE CENTRAL
NERVOUS SYSTEM
Creutzfeldt-Jakob disease (CJD) Fatal encephalopathy due to prions (proteinaceous material
(see Fig. 25-25) lacking RNA and DNA); in CJD, normal prion protein (PrP)
in neuronal membranes misfolds, becomes infectious, and
results in death of neurons (? apoptosis) and spongiform
change (cytoplasmic vacuoles; bubbles and holes);
infectious PrP resists standard sterilization techniques and
proteases.
Transmission: corneal transplants; grafts of dura mater;
improper handling of infected brain tissue; contaminated
deep implantation electrodes; ingestion of contaminated beef
from cattle with bovine spongiform encephalopathy (mad
cow disease)
Severe dementia; death usually occurs within 1 year

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Margin note last one on bottom: CPM: due to rapid IV correction of hyponatremia (usually in an
alcoholic)

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Margin note 1st on top: Krabbes disease: LSD; deficiency -galactocerebrosidase with in -
galactocerebroside in lysosomes
Margin note 4th from top: AD: phosphorylated A neurotoxic
Margin note 5th from top: Activated GSK-3: phosphorylates A

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Margin note 2nd from bottom: Wilsons disease: cystic degeneration of basal ganglia

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