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 Infection terminology:

 Contagious – highly communicable

 Subclinical – unapparent; only detected by demonstrating a rise in Ab titer (rising is the most reliable finding) or isolating the organism

 Latent state – absence of symptoms until a reactivation occurs

 Chronic carrier – organisms continue to grow w/ or w/out producing symptoms in the host

 Pandemic – worldwide distribution

 Endemic – constantly present at low levels in a specific population and with low incidence of infection

 Epidemic – occurs much more frequently than usual

 Swelling

 In an autopsy, cellular swelling (a commonly observed tissue change, is of little practical diagnostic imporance

 Cloudy swelling:

 Early degenerative change characterized by increase cytoplamsic granularity & increased size

 Swelling of cells due to injury to MBs affecting ionic transfer; causes an accumulation of intracellular water

 Shy-drager syndrome (multiple system atrophy)

 Rare degenerative condition w/ symptoms similar to Parkinson’s – pt may move slowly, be tremulous, & have shuffling gait

 Wiskott-Aldrich syndrome (aka immunodeficiency w/ eczema & thrombocytopenia):

 Affects only boys

 Characterized by defective B-cell & T-cell functions, Just like SCID mouse

 Clinical features – thrombocytopenia w/ severe bleeding, eczema, recurrent infection, & increased risk of lymphoid cancers

 Ataxia-telangiectasia:

 Inherited disorder that affects many tissues & body systems

 Multiple symptoms – telangiectasis (dilation of capillaries), ataxic (uncoordinated) gait, infection prone, defective humoral &

cellular immunity, & increased risk of malignancies

 Most obvious symptoms – multiple easily visible telangiectases in the sclera & skin areas such as ear & nose, graying of the hair, & irregular pigmentation of areas exposed to sunlight

 Decreased coordination of movement (ataxia) in late childhood

 Hyper-IgE syndrome (Job syndrome): -- JOB even got ALLERGIES

 Immunodeficiency disorder characterized by very high levels of IgE Ab/s & repeated infections (commonly w/ S. aureus)

 Tx – continual administration of Abx

 Calcification abnormalities:

 Metastatic calcification:

 Calcification occurring in nonosseous, viable tissue – stomach, lungs, & kidneys

 Cells of these organs secrete acid materials & under certain conditions in instances of hypercalcemia, the alteration in pH seems to cause precipitation of calcium salts at these sites

Occurs particularly in hypercalcemia, hyperparathyroidism & hypervitaminosis D, NOT hypoparathyroidism

 Pathologic calcification:

 Calcification occurring in excretory or secretory passages as calculi (in tissues other than bone & teeth)

 Eggshell calcification:

 Thin layer of calcification around an intrathoracic lymph node, usually silicosis, seen on a chest radiograph

 Dystrophic calcification:

 Deposition of calcium in dying or dead tissues

 Occurs in degenerated or necrotic tissue, as in hyalinized scars, degenerated foci in leiomyomas, & caseous nodules

 Secondary to disease of affected tissue

 NOT associated w/ high blood calcium levels

Unlike Metastatic Calcification

 Calcinosis:

 Presence of calcification in or under skin – often associated w/ scleroderma & sometimes dermatomyositis

 Staghorn stones:

 Occupy renal pelvis & calyces – big stones!

 Hematuria:

 Blood in urine – should never be ignored!!

 Usually caused by kidney & urinary tract disease

 Exceptions:

 Women – blood may appear to be in urine when it is actually from the va-jay-jay

 Men – blood mistaken for urinary bleeding is sometimes a bloody ejaculation due to prostate problems

 Children – coagulation disorders (e.g., hemophilia) or other hematologic problems (e.g., sickle cell disease, renal vein thrombosis, or thrombocytopenias) can be underlying reasons for newly discovered blood in urine

 Kidney disease following strep throat is a classic cause of hematuria

 Hematemesis:

 Vomiting of bright red blood – indication rapid upper GI bleeding

 Commonly associated w/ esophageal varices (common in alcoholics) or peptic ulcers

 Hemoptysis:

 Coughing up blood from respiratory tract

 Blood-streaked sputum often occurs in minor upper respiratory infections or in bronchitis

 Can also be seen in pts suffering from tuberculosis, lobar pneumonia (Diffuse, rusty sputum, S. pneumoniae), or bronchogenic carcinoma (NOT emphysema)

 Also can be seen in pts w/ a pulmonary embolism

 Hemoptysis is the main symptom of idiopathic pulmonary hemosiderosis (iron in the lungs)

 Glucosuria:

 Presence of glucose in urine – common in diabetes

 Ketonuria:

 Presence of ketones in urine – produced by starvation, uncontrolled diabetes, usually Type I, & occasionally alcohol intoxication

 Proteinuria:

 Presence of protein in urine – usually a sign of kidney disease

 Accumulation of endogenous pigments:

 Bilirubin

 Hemosiderin

Iron containing protein derived from ferritin, which is an iron storage protein

 Melanin – formed from tyrosine, synthesized in melanocytes

 Increased melanin pigmentation – seen in Addison’s disease

 Decrease melanin pigmentation – seen in albinism & vitiligo, and PKU

 Histiocytosis X (aka Langerhans Cell Histiocytosis & Differntiated Histiocytosis)

 FIXED macrophages

 Group of disorders in which histiocytes (scavenger cells) proliferate, esp. in bones & lung, often causing scars to form

 Characterized by abnormal increase in # of histiocytes – includes monocytes, macrophages, & dendritic cells

 Eosinophilic granuloma:

 Most benign form

 More common in males ~20 y.o.

 May be totally asymptomatic – there may be local pain or swelling

 In the mouth, Mn is most likely affected – loose teeth on affected side w/ signs of gingivitis

 Letterer-Siwe disease:

 Affects infants (< 2 y.o.) – fatal

 Child develops a skin rash w/ persistent fever & malaise

 Anemia, hemorrhage, splenomegaly, lymphadenopathy, & localized tumefaction over bones are usually present

 Oral lesions are uncommon

 Hand-Schuller-Christian disease:

 Occurs early in life, usually before 5 y.o. – more common in boys

 Triad of symptoms – 1) exophthalmos, 1) diabetes insipidus, 3) bone destruction (skull & jaws are affected)

 Oral signs – bad breath, sore mouth, & loose teeth

 Treatment – radiation & chemotherapy (poor prognosis)

 Habermann’s disease:

 Is not an example of Histiocytosis X

 Sudden onset of a polymorphous skin eruption of macules, papules, & occasionally vesicles w/ hemorrhage

 Polymyalgia rheumatica:

 Condition causing severe pain & stiffness in muscles of neck, shoulders, & hips

 Hydatidiform Mole

 A pathologic ovum (“empty egg” – ovum with no DNA) resulting in cystic swelling of chorionic villi and proliferation of chorionic epithelium (trophoblasts)

 Most common precursor of choriocarcinoma

 High beta HCG

 “Honeycombed uterus, cluster of grapes appearance

 Genotype of a complete mole is 46, XX and is purely paternal in origin (no maternal chromosomes); no associated fetus

 Partial mole is commonly triploid or tetraploid.

 Uterine Pathology

 Endometriosis

 Non-neoplastic endometrial glands/stroma in abnormal locations outside the uterus

 Characterized by cyclic bleeding from ectopic endometrial tissue resulting in blood-filled, chocolate cysts

 Ovary is most common site

 Clinically is manifest by severe menstrual related pain

 Often results in infertility

 Endometrial Hyperplasia

 Abnormal endometrial gland proliferation usually caused by excess estrogen stimulation

 Increased risk for endometrial carcinoma

 Most commonly manifest clinically by vaginal bleeding

 Endometrial Carcinoma

 Most common gynecologic malignancy

 Peak age is 55-65

 Clinically presents with vaginal bleeding

 Typically preceded by endometrial hyperplasia

 Risk factors  prolonged estrogen use, obesity, DM, and HTN

 Polycystic Ovarian syndrome

 Increased LH due to peripheral estrogen production leads to anovulation

 Manifest clinically by amenorrhea, infertility, obesity, and hirsutism

 Tx with weight loss, OCPs, gonadotropin analogs, or surgery

 Leiomyoma (See “Neoplasm’ section)

 Leiomyosarcoma (See “Neoplasm’ section)

 Breast Disease

 Fibrocystic Disease

 Presents with diffuse breast pain and multiple lesions, often bilateral

 Bx shows fibrocystic elements

 Usually does not indicate increased risk for CA, although it is a risk factor

 Histological types

• Cystic – fluid filled

• Epithelial Hyperplasia – Increase in number of epithlelial cell layers in terminal duct lobule, Increase risk for CA

• Fibrosis – Hyperplasia of breast stroma

• Sclerosing – Increased acini and intralobular fibrosis

 Benign Tumors

 Cystosarcoma phyllodes – large, bulky mass of CT and cysts, breast surface has “leaflike” appearance (“I love Fall”)

 Fibroadenoma – most common tumor <25 yrs, small, mobile, firm mass with sharp edges, increases with pregnancy

 Malignant Tumors

 Comon Postmenopause

 Arise from mammary duct epithelium or lobular glands

• Histologic types

♦ Comedocarcinoma – Cheesy consistency of tumor tissue due to central necrosis

♦ Infiltrating ductal – most common carcinoma, Firm, fibrous mass

♦ Inflammatory – lymphatic involvement, poor Px

♦ Paget’s disease – Eczematous patches on nipple

 Risk Factors  Gender, age, early menarche, delayed first pregnancy, late menopause, family history of 1st-degree relative with breast cancer at a young age, but NOT fibroadenoma or nonhypplastic cysts

 Wegener’s Granulomatosis

 Characterized by focal necrotizing vasculitis and necrotizing granulomas in the lung and upper airway and by necrotizing glomerulonephritis

 Symptoms  Perforation of nasal septum, chronic sinusitis, otitis media, mastoiditis, cough, dyspnea, hemoptysis

 Findings  C-ANCA is strong marker of disease, CXR may reveal large nodular densities, hematuria and red cell casts

 Tx  corticosteroids nad methotrexate

 Alcoholism

 Physiologic tolerance and dependence with symptoms of withdrawal (tremor, tachycardia, HTN, malaise, nausea, delirium tremens) when intake is interrupted

 Continued drinking despite medical and social contraindications and life disruptions

 Ethanol  via Alcohol Dehydrogenase and MEOS  Acetaldehyde  Acetate  Acetyl-CoA  Increased FAs  Fat Liver

• Alcohol Dehydrogenase

♦ Increases NADH/NAD+ ratio, which in turn:

 Basically tricks your body into thinking you have energy

 Increases Lactate/pyruvate

 Inhibitis gluconeogenesis

 Inhibits FA Oxidation

 Inhibits Glycerophosphate dehydrogenase, leading to elevated glycerophosphate

 Complications of Alcoholism

 Alcoholic Cirrhosis

• Long term alcohol use leads to micronodular cirrhosis with accompanying symptoms of jaundice,

hypoalbuminemia, coagulation factor deficiencies, and portal hypertension, leading to peripheral edema, ascites, encephalopathy, and neurologic manifestations

 Wernicke-Korsakoff Syndrome

Caused by Vitamin B1 (thiamine) deficiency in alcoholics

• Classically may present with triad of psychosis, ophthalmoplegia, and ataxia

• May progress to memory loss, confabulation, confusion (Irreversible)

• Associated with periventricular hemorrhage/necrosis, especially in mamillary bodies

• Tx with IV Vitamin B1

Mallory-Weiss Syndrome

DRUNK DUCKS

Longitudinal lacerations at the gastroesophageal junction caused by excessive vomiting with failure of LES relaxation that could lead to fatal hematemesis

 A Quick Review on Pathology Findings

 Argyll-Robertson Pupils

 Constricts with accommodation but is not reactive to light, pathognomonic for Tertiary syphilis

 Think ARP  Argyll-Robertson Pupil, Accommodation Response Present

 Amyloidosis

 Primary seen with multiple myeloma or Wadenstrom’s macroglobulinemia

 Secondary can cause nephrotic syndrome in kidney, Apple-green birefringement on Congo Red stain

 Alzheimer’s disease associated with Beta-amyloid deposition in the cerebral cortex

Islet cell amyloid deposition characterisitic of DM Type II

 Aschoff Body

 = Granuloma with Giant cells are also found with Anitschkow’s cells (activated histiocytes) in Rheumatic Heart Disease

Think 2 RHussians  Rheumatic

 Auer bodies

 Cytoplasmic inclusions in granulocytes and myeloblasts

 Primarily seen in Acute Myelocytic Leukemia -- Ambulance

 Casts (in Urine)

 RBC  glomerular inflammation, ischemia, or malignant HTN, Bladder Cancer

 WBC casts  inflammation in renal interstitium, tubules and glomeruli, Acute cystitis

 Hyaline casts  often seen in normal urine

 Waxy casts  Seen in chronic renal failure

 ESR (Sed Rate)

 Nonspecific test that measures acute-phase reactants

 Dramatically increased with infection, malignancy, CT disease, with pregnancy, inflammatory disease, anemia

 Decreased with Sickle cell anemia, polycythemia, CHF

 Hyperlipidemia signs

 Atheromata  Plaques in blood vessel walls

 Xantheloma  Plaques or Nodules composed of lipid-laden histiocytes in the skin, especially the eyelids

Tendinous Xanthoma  Lipid deposit in the tendon, especially Achilles,

 Familial Hypercholesterolemia

 Corneal arcus  Lipid deposit in cornea, nonspecific (arcus senilis)

 Psammoma bodies

 Laminated, concentric, calcific spherules seen in

Think PSaMMoma  Papillary adenocarcinoma of thyroid, Serous papillary cystadenocarcinoma of ovary, Meningioma, Malignant Mesothelioma

 RBC Forms

 Biconcave Normal

 Spherocytes Hereditary Spherocytosis, Autoimmune hemolysis

 Elliptocyte Hereditary Elliptocytosis

 Macro-ovalocyte Megaloblastic anemia, marrow failure

 Helmet cell, Schistocyte DIC, traumatic hemolysis

 Sickle cell Sickle cell anemia

 Teardrop cell Myeloid metaplasia with myelofibrosis

 Acanthocyte Spiny appearance in abetalipopreteinemia

 Target cell Thalassemia, liver disease, HbC

 Poikilocytes Nonuniform shapes in TTP/HUS, microvascular damage, DIC

 Burr cell TTP/HUS

 HLA-B27

 Think PAIR  Psoriasis, Ankylosing spondylitis, Inflammatory bowel disease, Reiter’s syndrome

 Virschow’s (sentinel) node

 Firm Supraclavicular lymph node, often on left side, easily palpable, also known as jugular gland

 Presumptive evidence of malignant visceral neoplasm (usually stomach)

 Random Qs All of the following should be HIGHLIGHTED YELLOW

 Bacteria surviving in CO2

 Capnophiles or Anaerobics -- think????

 Tran has another Q stating Anaerobics need CO2 to grow

 Retrovirus causes what in infants????

 Pneumonia, T-cell leukemia????

 Mushroom Toxins

 The recent answer was some Alpha-amanitin Toxin

 Ehler-Danlos Syndrome

 a group of inherited generalized connective tissue diseases characterized by overelasticity and friability of the skin, hypermobility of the joints, and fragility of the cutaneous blood vessels and sometimes large arteries, due to deficient quality or quantity of collagen;

 the most common is inherited as an autosomal dominant trait; some recessive cases have hydroxylysine-deficient collagen due to deficiency of collagen lysyl hydroxylase, and two tentatively ascribed to X-linked inheritance.

• Also associated with Berry Aneurysms

 What does CD stand for??

 Not compact disc, but Cluster of Differentiation

 They are surface molecules that are recognized by specific types of antibodies

 CD 4 and CD 8--- Ring a bell?

 Respiratory Burst

 The rapid release of SUPEROXIDE anion when PMNs come in contact with bacteria

 Throat Cancer

 Most are squamous cell carcinomas – Just like Skin and Esophagus

 Oral Cancer

 Occurs on the side of the tongue

 Tracheomalacia

 Trachea collapsing

 Noma

 Gangrenous disese of the mouth and cheeks

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