Hi-Yield Compendium Section 1.7 - 3.1

Front 1

Autoantibody of autoimmune hemolytic anemia

Back 1

Anti-RBC

Front 2

Autoantibody of Bullous pemphigoid

Back 2

Anti-epidermal basement membrane

Front 3

Autoantibody of Type I diabetes mellitus

Back 3

Anti-islet cell

Front 4

Autoantibody of pemphigus

Back 4

Anti-karatinocyte junction

Front 5

Autoantibody of pernicious anemia

Back 5

Anti-intrinsic factor, anti-parietal cell

Front 6

Autoantibody of microscopic polyangiitis

Back 6

p=ANCA

Front 7

Autoantibody of polymyositis

Back 7

speckled ANA

Front 8

Autoantibody of progressive systemic sclerosis

Back 8

Anti- Scl 70

Front 9

Autoantibody of sjogren's syndrome

Back 9

Anti - SS and and anti-SS B

Front 10

Autoantibody of idiopathic thrombocytopenic purpura

Back 10

anti-structrual platelet

Front 11

Autoantibody of vitigligo

Back 11

anti-melanoctye

Front 12

Autoantibody of rheumatoid arthritis

Back 12

Anti-IGG

Front 13

Autoantibody of SLE

Back 13

anti-nuclear antibody of rscreen, anti-ds DNA for confirmation

Front 14

Autoantibody of drug induced lupus

Back 14

anti-histone

Front 15

CREST

Back 15

anti-centromere

Front 16

Autoantibody of myasthenia gravis

Back 16

anti-ach receptor

Front 17

Autoantibody of graves' disease

Back 17

anti-tsh receptor

Front 18

Autoantibody of hashimoto's thyroiditis

Back 18

Autoantibody of anti-microsomal

Front 19

Autoantibody of wegener's granulomatosis

Back 19

anti-neutrophil cytoplasm

Front 20

Autoantibody of celiac sprue

Back 20

anti-gliadin

Front 21

Autoantibody of goodpasture's syndrome

Back 21

anti-glomerular basement membrane

Front 22

Autoantibody of primary biliary cirrhosis

Back 22

anti-mitochondrial

Front 23

Amyloidosis

Back 23

diseases with the depoition of amyloid protein. Diseases that cause local deposition of amyloid cause localized amyloidosis and those that cause systemic deposition cause systemic amyloidosis.

Front 24

Type I hypersnesitivity

Back 24

Triggerss: pollens, drugs, food, insect venom, animal dander.

Front 25

Type II hypersensitivity

Back 25

blood antigens during tranfusion, Rh antigens on fetal RBCs when mom is Rh-, drugs that attach to RBC membranes or platelet membranes, drugs that change host tissue, infectious agents, molecular mimicry, autoimmunity

Front 26

Type III hypersensitivity

Back 26

Drugs, vaccine, inhaled antigens, such as fungus

Front 27

Type IV

Back 27

Delayed: poision ivy, posion oak, nickel, soaps, mycobacterial infection, transplanted tissue
T-cell mediated: cytotocicity: transplanted or virus-infected cells and tissue, tumor cells

Front 28

Hyperacute transplant rejection

Back 28

Preformed antibodies bind to antigen on tissue. it is a type II hypersensitivity and time to onset is minutes to hours.

Front 29

acute transplant rejection

Back 29

memory T cells recognize antigen; cd8s destroy the grafts. Type IV and occurs days to months

Front 30

Chronic transplant rejection

Back 30

Antibodies develop over time, damage graft vasculature. Types II and III

Front 31

Graft vs Host transplant rejection

Back 31

T cells in transplanted tissue attack host.

Front 32

Oncogenes and tumor suppressor genes

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Activated oncogenes caused by uncontrolled cell division and mutated/lost tumor suppressor genes allowed uncontrolled cell division.

Front 33

Important oncogenes: c-myc

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Burkitt lymphoma

Front 34

Important oncogenes: c-abl

Back 34

chronic myelogenous leukemia

Front 35

Important oncogenes: ras

Back 35

colon carcinoma

Front 36

Tumor supressor genes BRACA-1

Back 36

breast and ovarian cancer

Front 37

Tumor supressor genes p53

Back 37

Breast, colon, and lung carcinomas

Front 38

Tumor Markers: alpha-fetoprotein AFP

Back 38

High: hepatoma, multiple gestation, neural tube defects, yolk sac tumor/endodermal sinus disease
Low: Downs

Front 39

Tumor Markers: PSA

Back 39

Prostate specific antigen

Front 40

Tumor Markers: CEA

Back 40

Carcinoembryonic antigen

Front 41

Tumor Markers: Acid phosphatase

Back 41

prostate cancer

Front 42

Tumor Markers: alkaline phosphatase

Back 42

Diagnose non-neoplastic disease too. Produced in bone, kidneys, placenta, biliary system

Front 43

Autosomal dominant

Back 43

Never skips generations

Front 44

X-linked dominant

Back 44

No male to male transmission and never skips generations

Front 45

X-linked recessive

Back 45

no male to male transmission

Front 46

autosomal recessive

Back 46

variables

Front 47

Questions to ask yourself

Back 47

Are any generations skipped? Is there any male to male transmisison of the gene?

Front 48

De novo mutation

Back 48

new mutation, parents are healthy but one of the progeny undergoes a spontaneous mutation.

Front 49

Mitochondrial inheritance

Back 49

These genes are only trasmissted to females and trasmitted to all of her children, females and males.

Front 50

Cystic fibrosis

Back 50

Most common lethal genetic disease of Cuacasians due to a mutation in the cystic fibrosis transmembrane conductance regulator gene. Characterized by a defect in chloride transmembrane movement in epithelial cells. Some clinical findings: meconium ileus, viscous mucus, recurrent respiratory infections, high NaCl in sweat and tears, chronic pancreatitis, cholelithiasis, malnutrition.

Front 51

Phenylketonuria

Back 51

Unable to metabolize phenylalanine, causig a build up of phenylalanine breakdown products and the inability to make melanin and the neurotransmitters nerepinephrine and dopamine. Results in neurotoxcitiy from phenylalanine breakdown products, results in lighter complexion due to decreased melanin synthesis.

Front 52

Albinism

Back 52

inability to make melanin

Front 53

alpha1-antitrypsin deficiency

Back 53

alpha1-antitrypsin normally functions to inhibit elastase. In this disease, the liver makes it but is unable to release it from its cells; liver destruction results. The active elastase destroys primarily the lung, resulting in emphysema.

Front 54

Thalassemias, sickle cell anemia

Back 54

abnormally structred hemoglobin, resulting in TBC defects that cause RBC destruction

Front 55

Glycogen storage diseases

Back 55

Von Gierke disease, pompe diseases, and mcardle disease. Inability to utilize glycogen normally Glycogen is a storage form of glucose.

Front 56

Mucopolysaccharidosis

Back 56

1 type of lysosomal storage disease. Unable to metabolize glycosaminoglycans. Different forms do or don't cause mental retardation or corneal clouding. Three types: Huler, Scheie, Hunter.

Front 57

Sphingolipidoses

Back 57

1 type of lysosomal storage disease. Unable to metabolize sphingolipids, molcules typically involved with myelin and the CNS.

Front 58

Polycystic kidney disease

Back 58

kidney cysts and liver cysts in infant; fatal

Front 59

Hemochromatosis

Back 59

Small intestine takes up excessive iron, even with normal diet. Excess iron deposits in liver, pancrease, herat, and skin- resulting in cirrhosis, new onset type i like diabetes, cardiomyopathy, and bronze colored skin. Bronze diabetes.

Front 60

Chediak-higashi syndrome

Back 60

WBCs have abnormal microtubules. Clinically see recurrent infections, development of lymphoid cancers, partial albinism, and neuropathy.

Front 61

Bernard-Soulier Disease

Back 61

Result sin excessive bleeding. Due to lack of GpIb

Front 62

Glanzmann's Thrombasthenia

Back 62

Results in excessive bleeding. Due to lack of Gp2b3a, which is needed for platelet to platelet adhesion.