Clinical Integration Flashcards Preview

Exam 2 > Clinical Integration > Flashcards

Flashcards in Clinical Integration Deck (65):
1

What are the 6 major categories of integral membrane proteins?

Pumps, channels, receptors, linkers, enzymes, and structural proteins

2

Cystinuria

Hereditary condition caused by abnormal carrier proteins that are unable to remove cysteine from urine, which causes kidney stones

3

Tetrodotoxin

Produced by puffer fish. Inactivates the sodium channels by occupying the sodium binding sites in nerve, paralyzing their prey (no action potential). Neurotoxin that leads to dizziness, ataxia, respiratory and death.

Membrane protein disorder.

4

Cholera

Exotoxin produced by vibrio cholera. Alters Gs protein so that it is unable to hydrolyze it's GTP molecule. This increases cAMP levels in the surface cells if the intestine, leading to excessive sodium ions and water loss, leading to diarrhea.

Membrane protein disorder.

5

Venoms

Inactivate acetylcholine receptors located on the skeletal muscle sarcolemma at neuromuscular junctions

Membrane protein disorder.

6

Autoimmune diseases

Produced antibodies that specifically bind to certain plasma membrane receptors causing them to become activated (hyperthyroidism in Grave's disease)

Membrane protein disorder.

7

Hereditary Spherocytosis

Genetic defect that is characterized by fragile, misshaped RBCs (Spherocytes). This results from a defective spectrum that have decreased ability to bind to band 4.1 protein. Leads to anemia because RBCs are being destroyed in the spleen

membrane protein disorder.

8

Cystic Fibrosis

AR disorders caused by a mutation in the CFTR gene on chromosome 7. Leads to exocrine glands secreting abnormally viscid mucus because the Chloride channels are defective

Membrane protein disorder

9

Downs Syndrome

Extra chromosome at 21. Characterized by mental retardation, short height, stubby appendages, and congenital heart defects. Can lead to early onset Alzheimer's

10

Klinefelters

XXY. Characterized by infertility, variable degree of masculinization, small testis.

11

Tuners Syndrome

XO. Short, sterile, and other abnormalities.

12

Transformed cells

Cells that have lost their ability to respond to regulatory signals controlling the cell cycle and may undergo division indefinitely (cancer)

13

Vinca Alkaloids

Arrest transformed cells in mitosis and keep them from replicating. Basis of chemo

14

P53

Cell cycle inhibit that stops the cycle and allows the nucleus to repair itself before moving on to division.

15

Lipoma

Very common benign tumor. usually found on the subcutaneous fatty tissue of the trunk or limbs. Soft, well defined lesions that are painless

16

Dysplasia

Repaid proliferation of epithelial cells with failure to differentiate

17

Carcinoma in situ

Carcinoma that is limited to the epithelia, does not invade the connective tissue.

18

Metaplasia

Complete reversible change of one mature epithelium with another. Example: Barrett's esophagus

19

Barrett's esophagus

Change in esophageal epithelium following damage

20

What is the function of lysosomes?

Digestion of macro molecules. they are stomachs or suicide bags

21

Lysosomal storage Diseases

Hereditary condition in which the synthesis of specific lysosomal acid hydrolase is impaired, meaning lysosomes cannot degrade certain components, interfering with cell function

22

Tay-Sachs

Lack hexosaminadase A (HexA) which digests glycolipids. Leads to build up of the lipid GM2 which shuts down the nervous system.

23

What are some symptoms of Tay-Sachs?

Enlarged head due to build up of storage in the brain, concentric lamellar bodies, increased muscle tome, and exaggerated Moro reflex. Characteristic cherry-red macular spot

24

Glycogen Storage Disease

Lysosomal storage disease. Leads to build up of glycogen in the liver and muscle

25

Hurler's Syndrome

GAGs accumulate in many tissues and organs. Lysosomal storage disease

26

Kartagener's Syndrome

AR disorder involving mutation in genes that code for ciliary protein dynein. A patient with this lacks most of the inner and outer dynein arms.

27

What are some symptoms of Kartagener's?

Situs inversus-organ reversal due to faulty migration during embryogenesis
recurrent pulmonary infections-inability to move mucus
Sterility in males-retarded sperm movement

28

What connects the basale to the basal membrane?

Hemidesmosomes

29

What connects keratinocytes?

Desmosomes

30

What is the normal rate of it over for cells?

2-4 weeks. It takes 2-4 weeks for cells to move from the bottom to the top where they are sloughed off

31

Transdermal Patch

Patch that is used as a means of delivering medication through the skin (Nicotine patch, steroid patch)

32

Epidermal would healing

Basal cells of epidermis surround the would, break contact with the basement membrane, and migrate across the wound. Migration stops when the cells tough each other (contact inhibition)

33

Epidermal Growth Factor

Stimulates basal stem cells to divide and replace the lost cells that have moved to the wound. They will divide and thicken the new epithelium

34

4 phases of Deep Wound Healing

Inflammatory, migratory, proliferative, maturation

35

Inflammatory Phase

Blood clot attached loosely to the edge of the cut. Vasodilation and increased permeability allow neutrophils and monocytes to enter the area and eliminate microbes and dying tissue

36

Migratory Phase

As the clot becomes a scab, epithelial cells migrate beneath it to bridge the wound. Fibroblasts synthesize scar tissue and damaged vessels regrow. This is granulation tissue

37

Proliferative Phase

Growth of epithelial tissue at random. Continued growth of vessels

38

Maturation Phase

Scab sloughs off. Epidermis is restored to normal thickness. Collagen is more organized. Fibroblasts decrease. This is a fibrosis scar.

39

What makes up fibrosis scar tissue?

Collagen and glycoprotein

40

Hypertrophic Scar

Scar that is more raised than normal, but within the normal boundaries

41

Keloid Scar

Scar in excess of the boundary

42

Hyperkeratosis

Hyperplasia of the horny layer (stratum corneum) of the skin or cornea

43

Parakeratosis

Retention of nuclei in the stratum corneum of the skin

44

Acantholysis

Loss of intracellular connections resulting in loss of cohesion between keratinocytes

45

Acanthosis

Epidermal hyperplasia in the stratum Spinosum

46

Complement System

Group of proteins that effect lysis of cells and Ag-Ab complexes

47

Psoriasis

Increased rate of proliferation of mitosis cells leading to a thickened epidermis, leading to shedding of the epidermis. Chronic inflammatory and proliferative disorder

48

Bullous Pemphigoid

Chronic, auto-immune blistering disease in the skin and mucous membranes.

49

What causes bullous Pemphigoid?

Autoantibodies specific for hemidesmosomes bind to the basement membrane and stimulate leukocytic infiltration. Eosinophils then release proteases that degrade hemidesmosomes and blisters form

50

Bulla

Large, fluid filled vesicle

51

Pempighus Vulgaris

Rare autoimmune disordered affecting the epidermis and mucosal epithelium. Disrupts desmosomes, leading to a separation of epidermal cells and atrophy of the prickle layer. Blisters form, giving a fish net appearance.

52

Pemphix

Blister/bubble

53

Albinism

Autosomal recessive. Loss of pigmentation of the skin, hair, and eyes. Results from a mutation in genes that regulate melanin synthesis and distribution of melanocytes inhibiting their ability to pick up tyrosine (tyrosine leads to DOPA which creates melanin)

54

Ocular Albinism

Eyes effected

55

Oculocutaneous Albinism

Eyes and skin pigment

56

Vitiligo

Autoimmune dipigmentation disorder leading to the destruction of melanocytes.

57

What are some treatments for vitiligo?

Topical steroid therapy, photo chemotherapy, dipigmentation, skin graft, micro pigmentation, melanocytes transplant

58

Squamous Cell Carcinoma

Malignant tumor of keratinocytes caused by DNA damage from UV (P53 inactivated). Leads to hyperkeratosis and parakeratosis

59

What are some factors that increase your likelihood to get squamous cell carcinoma?

Age (older than 70), skin color (fair skinned more likely) tobacco, carcinogens, radiation

60

Squamous Pearls or Swirls

Islands in the skin with undifferentiated cells resembling basal cells around the perimeter. Cauliflower like growth.

61

Basal Cell Carcinoma

Caused by UV light. Growth has rolled out margins.

62

Palisade Arrangement

Basal cells are arranged around tumor cells like a fence

63

Malignant Melanoma

Exposure to UV lights caused an increased number of melanocytes with large, atypical morphology arranged at the demo-epidermal junction. If it invades the dermis, it can be fatal.

64

ABCs to clinical diagnosis of spots on skin

Asymmetry
Border Irregularity
Color variation
Diameters (>6mm)
Elevation or evolving of current lesion

65

What is another name of neurofibromatosis?

Von recklinghausens disease (not a skin disease!)