things I keep forgetting

meteaplasia

change in type

-one gets swapped out (smoker’s airway)—handle the damage but lose some functions

-reversible

dysplasia

deranged growth

-precursor

liver transplant regrowing?

hyperplasia

how do free radicals harm cell?

-they want an electron and will do whatever to get it. this damages cells

which cell death is inflammatory?

necrosis

which cell death is NOT causing inflammation

apoptosis

talk about cell injury and hypoxia

so cell doesn’t have o2 so the cell switches over to anaerobic (not as effective), thus producing lactic acid (bad). this burns through glycogen storage quickly, and results in no more ATP. This makes the pumps not work, specifically NaK. Na floods cell, bring water w/ it and cell swells.

5 s/s of inflammation

pain, red, swelling, loss of function, heat,

what kicks off vasodilation w/ injury?

histamine

vascular stage components (3)

histamine triggers vasodilation (open the highway), increased permeability (lets extra people in), and outflow of fluid (full cell)

chemotaxis

trail to the infection (chemokymes)

opsinization

flagging the bad cells so phagocytes know who to eat/kill

cellular stage—explain

so now the cells are all in there, and its crowded. so blood is slowed down and bad cells can get trapped. then PMM (poly morphic ____—specifc WBC) drift towards the edge of problem (margination) , then stick to the side of the vessel (adhesion). and they squeeze into holes to get the bad guys (chemotaxis). now time to kill. there is a thing called opsinization (coding the bad guy—CB3). then phagocytosis (kill it). lysosomes use enzymes to kill it.

where is histamine stored?

mast cells

leukotrains

slow relaxation of smooth muscle (compared to fast acting histamine)

left shift—explain.

serious inflammation. so the bone marrow ramps up neutrophils and then sometimes in a rush, releases immature neutrophils—aka bands. you will see this on CBC w/ diff.

sepsis

cytokines overflow everywhere.leaky cells.

ESR

non-specific

-how quick RBC settle

CRP

more acute

interleukin 6

marfan

cardiac

neutrophil

most abundant

first responders

eat up bacteria and fungi w/ phagocytosis

types of granulocytes (3)

neutrophils, eosinophils, basophils

marfan is what kind?

autosomal dominant

Neurofibromatosis is what kind>

autosomal dominant

Neurofibromatosis—what cells

schwann

•Phenylketonuria (PKU) is what kind?

autosomal recessive

tay-sachs is what kind?

autosomal recessive

cleft lip, club foot, pyloric stenosis what kind?

multifactorial inheritance

trisomy 21

down’s

monosomy x

turner

polysomy X

Klinefelter

TORCH

toxoplasmis

other

rubella

cytomegalovirus

herpes

infectious during pregnancy

NK cells, complement system, phagocytes, epithelial cells part of what system

innate immunity

humoral immunity part of

adaptivec

cell mediated immunity part of?

adaptive immunity

humoral is what kinda cell?

B

cell

antibodies made in

humoral (b cell )

cell mediated are associated wih

T cell

what immunity makes phagocytes / pac men>

adaptive—cell mediated.

autoimmune is too much or too little?

too much—we no longer recognize ourselves as safe

peripheral lymph examples

lymph nodes, spleen, tonsils, appendix, peyer patches

immunoglobin are _______

antibodies

MALT

located around mucosa—anything exposed to outside junk. extra protection from outside stuff.

cytokines

they can increase/decrease inflammation

they do not kill themselves, they coordinate others.

short lived, very localized.

interleukin

interfere w/ viral replication

IgE

parasitic, allergic, hypersensitivity

IgD

found on B lymphocytes

IgA

saliva, nasal, respiratory secretions

IgM

immediate

activates complement

IgG

cross placenta, active 3-6m.

what cells make antibodies?

B cells

mature T cells are called?

CD4 (helper) and CD8 (cytoxic)

job of CD4 / t helper cell?

secrete cytokines and regulate who goes where

CD8 job?

kill things—trigger apoptosis (programmed death)—important w/ replication

what type of immunity is vaccination?

active

type 1 sensitivity—time, what happens?

immediate and first time w/ problem

IgE-mast and basophil activated

primary (5-30min)-histamine vasodilates and secondary responses (2-8hr)—time

—food, pollen, plants, etc.

type 2—who is involved? and example.

Antibody mediated response–Mediated by IgG or IgM–antibodies directed against antigens (usually on red or white BC)

1. Transfusion reactions, rH disease

type 3

Immune complex response

After vaccinations, glomerulonephritis–after strep a lot of time

1. glomer==filters. All this stuff comes into urine and then you get coca cola urine.

   1. Fish net isn’t good enough

2. Take a strep test—Glomerulonephritis

type 4 sensitivity

Cell mediated hypersensitivity disorder

T cell activation

1. Ex: transplant organ rejection

   1. Latex allergies

confirmatory HIV?

western blot

8 stages/phases of HIV—A flamingo rarely integrates telephone translation at meetings

1. attachment

2. fusion

3. reverse transcription

4. integration

5. transcription

6. translation

7. assembly

8. maturation

3 stages of HIV

acute, chronic, aids

melanocytes

color to skin

absence of melanocytes

vitiligo, albino

too much melanocytes

mongolian spot (butt cheeks), melasma

Tinea corporis

Cradle cap

Tinea faciale

Ringworm face

tinea incognito

w/ steroids

Tinea versicolor

1. Trunk

2. Wet hair on back–fungus likes water

Tinea capitis

scalp

Tinea pedis

Athlete’s foot

Tinea unguium

1. Nail fungus

2. Treated for 1yr

papule

solid, raised bump

vesicle

raised pocket—clear fluid

ex: chicken pox, herpes, contact dermitis

pustule

bump or blister—filled with yellow, pus

ex: acne, bacterial folliculitis

Impetigo

1. Small, honey crusted lesions, vesicles or pustules or bulla on face

Ecthyma

ulcerative form of impetigo

Human papillomavirus

Verrucae (warts) are common benign papilloma

herpes simplex virus Types

1. One: Saliva, droplets

2. Two: genital herpes

3 types UV rays

UVC, UVB, UVA

UVB rays

290 to 320 nm; responsible for nearly all the skin effects of sunlight

---

b for beach—where sunscreen

UVC rays

Short (100 to 289 nm); do not pass through the earth’s atmosphere

UVA rays

321 to 400 nm; can pass through window glass, are more commonly referred to as sun tanning rays

Atopic dermatitis

An inflammatory skin disorder that is characterized by poorly defined erythema, edema, vesicles, and weeping at the acute stage

Contact dermatitis

Allergic contact dermatitis results from a cell-mediated, type IV hypersensitivity response.

Irritant contact dermatitis is caused by chemicals that irritate the skin.

basal cell

most common skin cancer

skin and oral lesions that look like milky white lacework

Lichen planus

nevi

mole

wood’s light

fungal infection glow yellow-green

benign tumors grow by

expansion

malignant tumor

grow rapid, spread to distant body parts.disorganized, not well differentiated. s

malignant tumor spreads by

direct invasion, extension, seeding of cancer cells in cavities, metastatic spread

papillomas

benign microscopic or macroscopic finger-like projections growing on a surface

•Sarcoma:

malignant tumors of mesenchymal origin

•Carcinoma:

malignant tumor of epithelial tissue

protooncogenes

“gas pedal”

ABCDE mole

Asymmetry

Border

Color

Diameter

Evolving

most common child cancer

ALL

Wilmes tumor–

fast, kidney