• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/91

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

91 Cards in this Set

  • Front
  • Back
what are the FOUR major aspects of Pathology
1. Etiology: cause
2. Pathogenesis: mechanism
3. Morphologic changes: structural alteration in cells and organs
4. Clinical Sig: functional consequences (S/S, Course, Dx, Complications, Px)
what is the most common cause of cell injury in Clinical Medicine...THREE CAUSES??
HYPOXIA: due to insufficient blood supply to tissues (ischemia)

1. obstruction of arterial flow or venous drainage
2. inadequate oxygenation of blood owing to cardio-respiratory failure
3. loss of oxygen carrying capacity of blood (anemia)
lipofuscin...more prevalent in who??
yellow/brown wear and tear pigment caused by physical, chemical, or other injurious agents causing somatic mutation and changes in cell constituents
how does the body protect against oxidation
body produces superoxide dismutase (SODs), glutathione peroxidase and catalase

taking antioxidants (vit A, C, E) also helps
ubiquitin-proteasome system?
perform selective protein elimination to prevent cell injury and disease...operates under physiological and pathological processes
what are THREE nuclear changes in NECROSIS
1. pykosis: nucleus condenses into solid, shrunken basophilic masses
2. karyorrhexis: nucleus undergoes fragmentation
3. karyolysis: basophilia of chromatin fades and nucleus totally disappears

IRREVERSIBLE
what are the FIVE types of NECROSIS
1. Coagulative: happens everywhere except the brain
2. Liquefactive: primarily in the brain due to breakdown of myelin
3. Caseous: white, milky, amorphous material in tuberculous lesion
4. Enzymatic Fat: occurs when fats are digested by lipases and pooled
5. Gangrenous: dry and wet, also a type of coagulative necrosis
apoptosis
a distinct pattern of death of a single cells (distinct from necrosis)

suppression may be a determinant of growth of cancer
THREE causes of intracellular accumulation
1. excessive amounts of normal metabolites
2. abnormal nonmetabolizable substances
3. excessive intracellular synthesis of some products

REVERSIBLE!!
difference between:
1. dystrophic calcification
2. metastatic calcification
1. dystrophic:
calcium deposition in dead and dying tissues
normal calcium metabolism
normal serum level

2. metastatic:
calcium deposition in normal tissues due to hypercalcemia
abnormal calcium metabolism
SIX causes for HYPERCALCEMIA
M.I.S.H.A.P

1. Malignancy
2. Immobilization
3. Sarcoidosis
4. Hyperparathyroidism/Hypervitaminosis D
5. Alkalidosis/Addison Syndrome
6. Paget
what are SEVEN types of ATROPHY
1. Disuse: decreased workload
2. Denervation: muscle paralysis
3. Vascular: diminished blood supply
4. Nutritional: starvation
5. Endocrine: trophic hormones
6. Pressure: prolonged pressure
7. Senile: morphological changes of aging
what is the difference between hypertrophy and hyperplasia
1. Hyperplasia: increase in # of cells in a tissure w/ increase in size of organ
2. Hypertrophy: increase in size of tissue or organ due to increase in size of its component cells
FIVE characteristics of dysplasia
abnormality in maturation with variation in size, shape, orientation and organization of epithelial cells

1. increase in size of nucleus relative to that of cytoplasm (N:C ratio)
2. hyperchromasia
3. abnormal chromatin forming coarse clumping and irregular and thickened nuclear membrane
4. presence of NORMAL and ABUNDANT mitotic figures
5. disorderly maturation of cells

REVERSIBLE
what is the difference between benign and malignant tumors
benign
1. high degree of differentiation, resembles tissue of origin
2. expansile growth, compression of adjacent tissue and forms CAPSULE
3. slow rate of growth and it MAY stop
4. NEVER METASTASIZE

malignant:
1. varying degrees of undifferentiation and anaplasia
2. invade adjacent tissues, NO CAPSULE
3. rapid AND continual growth
4. spread via METASTASES
what is the difference between ANAPLASIA and DYSPLASIA
anaplasia shows all features of dysplasia

ANAPLASIA is a major microscopic characteristic of malignancy...DYSPLASIA is reversible
what are malignant tumors of the epithelium called...mesenchymal tissue
epithelium: CARCINOMA
mesenchymal: SARCOMA
what are the FOUR pathways of spread of MALIGNANT TUMORS
1. DIRECT LOCAL INVASION: tumor becomes fixed to the adjacent structure
2. TRANSCOELOMIC SPREAD: peritoneal cavity commonly involved (Krukenberg tumor from stomach to overies)
3. LYMPHATIC SPEAD
4. HEMATOGENOUS SPREAD: if systemic (if vena cava is involved then lungs are most common site), if portal venous system (liver, most common site), if arterial (brain, liver and bone
what is the difference between grading and staging of cancer
1. grading: based on degree of differentiation of tumor cells and number of mitoses present (1-4 with increasing anaplasia)
2. staging: based on size of tumor, extent of spread to regional lymph nodes, and the presence or absence of metastases. MORE CLINICALLY RELEVANT
what are the FOUR major viral oncogenic agents
1. hepatitis B group, HBV (liver)
2. HPV (papilloma in skin, larynx, genitalia) (carcinoma of uterine cervix and vulva)
3. Epstein-Barr (Burkitt lymphoma, Immunoblastic lymphoma, nasopharyngeal carcinoma)
4. Human T-cell Leukemia (Adult T-Cell Leukemia/lymphoma)

1-3 are DNA, 4 is RNA
what are the FOUR antioncogenes
1. Rb genes: normal genes product prevents cells from entering S phase of cell cycle
2. p53 gene: repair damaged DNA and induces apoptosis
3. BRCA 1&2: DNA repair
4. APC gene: A cell regulator gene
what are the NINE effects of tumor on host
A.C.H.O.I.S.E.P.U.T

1. Anemia
2. Cachexia
3. Hormonal effects
4. Obstruction
5. Irritation of serous membrane
6. SEcondary Infection
7. Produce a Lesion: SOL
8. Ulceration and bleeding
9. Torsion
what is the most important method of cancer diagnosis
HISTOLOGICAL EXAMINATION

still subjective though
what are the TWO most important tumor markers
1. alpha-fetoprotein (liver and testes)
2. carcinoembryonic antigen (colon, pancreas, lungs, stomach, breast)


NOT GOOD FOR Dx
important for monitoring to see if treatment is working or not
what is edema? what is the difference between transudate and exudate?
accumulation of abnormal amounts of fluids in intercellular tissues spaces or body cavities

transduate: NONINFLAMMATORY EDEMA fluid, LOW protein and colloids LOW specific gravity, FEW cells

exudate: INFLAMMATION, HIGH protein, HIGH specific gravity, MANY cells
THREE causes of EDEMA
1. increase in intravenous hydrostatic pressure
2. fall in osmotic pressure of plasma
3. impairment or obstruction of the flow of lymph
what happens when the pressure of the venous end is INCREASED (>12mmHg)
EDEMA

fluid will not return to the capillary
how does heart failure cause edema
INCREASE in hydrostatic pressure causing EDEMA
how does HYPOPROTEINEMIA cause EDEMA
hypoproteinemia will cause a DECREASE in osmotic pressure of plasma protein.

lower than 25mmHg, fluid can NOT enter back to the capillaries
what are FOUR clinical types (morphological) of edema
cardiac, renal, pulmonary, cerebral

1. cardiac: subcutaneous edema most prominent in lower extremities...pitting edema(NOT HEART)
2. renal: generalized, manifested initially in loose tissues such as eyelids, pitting edema
3. pulmonary: seen in LV FAILURE, renal failure and lung disease
4. cerebral
what is active hyperemia
1. increased arterial flow due to arteriolar dilation
2. seen in skin and muscles during exercise and at site of inflammation
what causes PULMONARY edema? what are the effects
causes:
1. LEFT VENTRICLE FAILURE
2. Rheumatic heart disease
3. floppy MV with regurgitation

effects:
1. HEART FAILURE CELLS (present in LUNGS not HEART)!!
2. pigmentation, brown induration of lungs
what causes LIVER edema? what are the effects
causes
1. RIGHT VENTRICLE FAILURE
can be ACUTE or CHRONIC

effects:
1.pigmentation, NUTMEG LIVER
what causes SPLEEN edema? what are the effects
causes:
PORTAL VEIN OBSTRUCTION

effects:
pigmentation, Gamma Gandi Bodies
what is Virchow's Triad
1. endothelial injury releases thrombotic/antithrombotic factors result in clotting (important disease is Atherosclerosis)
2. changes in Blood Flow
3. hyper-coagulability of Blood
what causes hyper-coagulability of blood
D.O.N.T.M.I.S.S.

1. Deficiency of antithrombin III or protein C
2. Oral Contraceptives
3. Nephrotic Syndrome
4. Trauma
5. Malignant cells secrete procoagulants
6. Increased # and Stickiness of platelets
what are the FIVE fates of thrombus
I.ROPE

1. Infection: thrombus may become infected
2. Removal: via fibrinolytic action
3. Organization and recanalization
4. Propagation: may cause obstruction
5. Embolization: whole or part of thrombus may break off

PROPAGATION and EMBOLIZATION is the WORST
what are the SIX clinical settings when a thrombus can occur
1. advanced age
2. bed rest and immobilization
3. heart disease
4. tissue injury
5. cancer
6. late pregnancy and delivery
what is usual impact for emboli arising from the veins? arteries
1. veins->lungs
2. arteries->legs, brain, systemic

99% of emboli are thrombi
what is significant about pulmonary embolism
MOST IMPORTANT
1. large embolus may block MPA or become saddle embolus (immediate death or right heart failure)
2. >95% of pulmonary emboli arises from DVT
what is the clinical significance of infarction
common cause of clinical illness and myocardial, cerebral and pulmonary infarctions are responsible for over HALF of all deaths
what are the four major causes of SHOCK
V.O.C.H.
1. Vasogenic
2. Obstructive
3. Cardiogenic
4. Hypovolemic
what are causes of hypovolemic shock
inadequate blood volume

1. hemorrhage
2. trauma
3. surgery
4. burns
5. fluid loss (vomitting/diarrhea)

particularly important in children
what are the causes of vasogenic shock (distributive)
increase size of vascular shock (vasodilation, NORMAL blood volume)

1. fainting (neurogenic shock)
2. anaphylaxis (allergies)
3. sepsis (vasodilation and increase capillary permeability)

peripheral pooling
NO BLOOD LOSS
blood not available for circulation
what are the causes of cardiogenic shock
decrease cardiac output

1. myocardial infarction (MI)
2. congestive heart failure (CHF)
3. arrhythmias (ventricular arrhythmia)
what are the causes of obstructive shock
obstructive blood flow

1. pulmonary embolism
2. cardiac tamponade
3. cardiac tumor
4. tension pneumothorax
what is the most common cause of death in the ICU
SEPTIC SHOCK (Vasogenic)

vasodilation and myocardial depression
what happens during an allergic reaction
ANAPHYLACTIC SHOCK

allergic reaction leads to a release in histamine causing vasodilation

DECREASE BLOOD PRESSURE
what are the THREE forms of SEPSIS
1. sepsis
tachycardia, tachypnea, inc/dec Temp, inc/dec WBC count

2. sepsis syndrome (sever sepsis): sepsis w/ decreased perfusion, peripheral dilation, hypoxemia. (also low lactate, low urine output, and low mental status)

3. septic shock: SS with hypotension despite fluid administration
what are the THREE important autosomal DOMINANT conditions
1. Marfan's Syndrome
2. Familial Hypercholesterolemia
3. Neurofibromatosis
what are the SIX important autosomal RECESSIVE conditions
GGCLAP

1. galactosemia
2. glycogenoses
3. cystic fibrosis
4. lysosomal storage diseases
5. albinism
6. phenylketonuria
Marfan Syndrome
1. type of disorder
2. what happens
3. clinical features
1. autosomal DOMINANT disorder
2. qualitative and quantitative defects in fibrillin
3. affect skeleton, eyes, cardiovascular sys.

high arched palate, bilateral dislocation of lens, retinal detachment, MV prolapse
Familial Hypercholesterolemia
1. type of disorder
2. what happens in homozygotes and heterozygotes conditions
1. autosomal DOMINANT disorder
2. LDL receptor id deficient

1. Homozygotes: develop Xanthomas in childhood and soon death via MI
2. Heterozygotes: cholesterol deposit along tendon shealths and premature atherosclerosis
Neurofibromatosis
1. type of disorder
2. what are the 3 major features of type 1.
autosomal DOMINANT disorder

1. multiple neurofibroma
2. pigmented skin lesions
3. pigmented iris hamartomas

type 2 (acoustic): rare, characterized by skin pigmentation
cystic fibrosis
1. type of disorder
2. what happens
autosomal RECESSIVE disorder

widespread defect in exocrine glands. clinically manifested by recurrent pulmonary infections and pancreatic insufficiency

REVIEW: exocrine glands secrete sweat, digestive juices and mucus
phenylketonuria
1. type of disorder
2. what happens
autosomal RECESSIVE disorder

1. deficiency or absent of hepatic enzyme, phenylalanine hydrooxylase (PAH)
2. result in failure conversion of dietary phenylalanine to tyrosine

PA levels in blood NORMAL at birth, but very high after 2nd week.
what are the FIVE main infectious causes of newborn morbidity
T.O.R.C.H.

1. toxoplasma
2. other
3. rubella
4. cytomegalovirus
5. herpes simplex
what are the THREE main causes of cytogenetic chromosomal disorders
1. increasing maternal age
2. ionizing radiation
3. drugs (anticancer agents, thalidomide, especially in early stage of pregnancy)
Klinefelter Syndrome
1. type of disorder
2. what happens
sex chromosome disorder

1. male hypogonadism
2. most patients with 47 XXY

small balls, ball atrophy, mild retardation, etc.
turner syndrome
1. type of disorder
2. what happens
sex chromosome disorder

1. female hypogonadism
2. 55% monosomy (45X) or 45% mixture 45X/46XX
what is the difference between cell mediated immunity and humoral immunity
1. cell mediated: defense against intracellular microbes
2. humoral: defense against extracellular microbes and their toxins
1. CD4+ T Cells associate with...
2. CD8+ T Cells associate with...
1. CD4+T cells associate with Class II MHC presentations
2. CD8+ T cells associate with Class I MHC presentations
where are the MHC clustered
clustered and produced on a small segment of CHROMOSOME 6
what tells the lymphocytes to activate, grow and differentiate
interleukin 2 and 4
what is an important ability of the natural killer cells
1. ability to lyse variety of tumor cells, virally infected cells, and some normal cells w/o activation
2. first line of defense against neoplasm or viral infections
3. can lyse IgG coated targets and MHC expressions
what are the TWO phase of type 1 hypersensitivity
1. initial: vasodilation and vascular leakage (happens within 5-30min)
2. late: tissue destruction, infiltration of WBC (eosinophils, neutrophils, basophils, monocytes) and CD4+ (2-8hrs)
in type 1 hypersensitivity what Ig does the antigen bind to and what does it cause
Asthma
1. antigen binds to IgE
2. signals leads to mast cell degranulation
what are the three categories of type 2 hypersensitivity
1. complement-dependent reaction: direct lysis and opsonization (blood allergy)
2. antibody-dependent cell mediated cytoxicity: cell lysis proceeds w.o. phagocytosis (tumor)
3. antibody-mediated cellular dysfunction (myasthenia gravis and graves disease)
what is the principle behind type 2 hypersensitivity
mediated by antibodies (IgG and IgM) directed towards antigens present on the surface of the cells or other tissue components
what happens in type 3 hypersensitivity
1. antigen-antibody complex formation
2. complement activation
3. phagocytosis
4. lysosomal enzyme release
5. tissue damage or systemic damage
what happens in type 4 hypersensitivity and what is a common procedure that involves this type of rxn
1. cell mediated hypersensitivity is initiated by specifically sensitized CD4+
2.involves direct cell cytotoxicity mediated by CD8+

TB SKIN TEST
what are the two mechanisms of host vs graft disease
1. T-cell mediated reactions: direct (tcell of recipient recognizes MHC of donor) and indirect (classic model)
2. Antibody-Mediated reactions: hyperacute (antidonor antibodies are already present in body of recipient)
what is the pathogenesis of SLE
1. generate antibodies against cell membrane (PhosphoLipid Bilayer)
2. Lupus anticoagulant prolongs PTT
3. causes false positive test result for Syphilis
how does SLE relate to Syphilis? Why?
1. FALSE POSITIVE FOR SYPHILIS
2. antibodies against the phospholipid-beta2-glycoprotein complex also bind to CARDIOLIPIN antigen
what is used a clinically diagnosis for SLE
presence of antibodies to dsDNA and the Smith antigen
what is Sjogren Syndrome
1. autoimmune disease
2. dry eye/dry mouth (sicca syndrome)
3. destruction/fibrosis of the lacrimal and salivary glands
what does the infiltrate activate in Sjogren Syndrome
CD4+ helper T Cells and some B cells
what is a clinically diagnosis for Sjogren
present of two ribonucleoproteins
1. SS-A (Ro)
2. SS-B (La)
detected in 90% of patients by highly sensitive techniques

Biopsy of the LIP!!!
what is systemic sclerosis and what are the TWO types??
autoimmune disease characterized by abnormal accumulation of fibrous tissue in the skin and multiple organs

1. diffuse: widespread, rapid progression and early visceral involvement
2. limited: limited to face, fingers, and forearm. visceral later...
what is C.R.E.S.T.?? what is it associated with??
LIMITED SCLERODERMA

Calcinosis
Raynaud phenomenon
Esophageal dysmotility
Sclerodactyly
Telangiectasia
what are the clinical diagnosis of systemic sclerosis
1. DNA topoisomerase I: highly specific, present in 28-70% of patients with DIFFUSE sys. sclerosis
2. Anticentromere antibody: is found in 22-36% of patients with LIMITED sys. sclerosis
what is X-linked Agammaglobulinemia of Bruton
1. failure of B-cell precursors to differentiate to B cells
2. block maturation due to mutation in cytoplasmic tyrosine kinase
3. apparent after 6 months, antibodies are depleted
4. H.influenzae, Strep.pneumoniae, Staph. aureus
what is thymic hypoplasia
DIGEORGE SYNDROME

1. T cell activation absent
2. infants are vulnerable to viral, fungal and protozoal infection
3. NO CD8 or CD4

NOTE: B CELL FUNCTION NORMAL
what is common variable immunodeficiency
1. hypogammaglobulinemia (very low levels of antibodies)
2. block in Bcell maturation to plasma cells
3. NORMAL NUMBER OF B CELLS
4. NO PLASMA CELLS
what is the most common immunodeficiency disease
isolated IgA deficiency
what is isolated IgA deficiency
1. block in terminal differentiation of IgA-secreting B cells to plasma cells

IgA is important in respiratory, and GI...so obviously block of IgA will cause these systems to malfunction
what is severe combined immunodeficiency diseases
1. defect in BOTH humoral and cell-mediated immune response
what is HIV envelope studded with?
viral glycoproteins
1. gp120
2. gp41
how does HIV enter the cells
viral glycoproteins (gp120 & gp41) interaction with CD4 receptor and chemokine receptors
what are the THREE phases of HIV infection
1. acute: 3-6 weeks, CD4 reduction, cold like symptoms
2. chronic: lymphadenopathy develops, CD4 declines further, thrush
3. crisis: you're screwed
what are the THREE diagnostic processes for HIV
1. ELISA: 99% sensitive (detect p24)
2. Western Blot: 2 bands (p24 & p41) (gp120 & gp160)
3. Viral Load: CD4 count