Summative 1

NSAIDS stands for

nonsteroidal anti-inflammatory drugs

autacoids act like

local hormones that trigger pain, inflammation, fever

autacoids produced by what

all cells

eicosanoids is a type of

autacoid

eicosanoids derived from

20C unsaturated fatty acid

eicosanoids - examples

prostaglandin, prostacyclin, thromboxane, leukotriene

eicosanoid - synthesis

phospholipase changes phospholipid into arachidonic acid > cyclooxygenase changes it into prostanoids

COX-1 - what, where

constitutive; in normal cells

COX-2 - what, where

inducible; in inflammatory cells

what leads to platelet aggregation

TXA

what inhibits platelet aggregation

PGI

what leads to smooth muscle relaxation and vasodilation

PGE

what leads to mucus

PGF2, PGE

what inhibits gastric acid secretion

PGI

what leads to respiratory smooth muscle relaxation

PGE, PGI

what maintains renal blood flow

PGE, PGI

tNSAIDS with a serious side effect are called

pyrazolidinediones

tNSAIDS - side effects

GI bleeding and ulcer, nephrotoxicity

tNSAIDS - adverse effects

gastropathy, renal failure, fluid retention, heart failure, liver injury

tNSAIDS - affect on plateletes

reduce aggregation

tNSAIDS - drug interactions (NSAID, ACE inhibitor, warfarin)

irritate GI; increased BP, bradycardia; bleed, toxicity

tNSAIDS - contraindications

peptic ulcer, GI bleeding, kidney disease

aspirin - name

acetylsalicylic acid

aspirin - difference

irreversibly inhibit COX

aspirin - effects

analgesic, antipyretic, anti-inflammatory

aspirin - low dose effects

reduced uric acid excretion leading to gout

aspirin - toxicity effects

hyperventilate, dehydration, renal failure, shock

aspirin - adverse effects

gastropathy, bleeding, nephrotoxicity, reye’s syndrome

Reye’s syndrome

brain and liver swell especially in children with viral infections

aspirin - contraindications

pregnancy, gout, bleeding, gastropathy

which NSAID is not associated with MI and stroke

aspirin

aspirin - toxicity treatment

induce vomit, sodium bicarbonate

selective COX-2 inhibitors - differences

decreased risk of GI effects, blood can still clot

celecoxib - contraindications

liver and kidney disease

celecoxib - effects

analgesic, antipyretic, anti-inflammatory

celecoxib - metabolized by

cytochrome P450

acetaminophen - effects

pain and fever relief

acetaminophen - what

weak COX inhibitor (1,2,3)

acetaminophen - affect on platelets

none

acetaminophen - used in

children with viral infection, peptic ulcer, GI bleeding, renal disease

acetaminophen - toxicity

quinone (NAPQI) accumulation > liver damage

acetaminophen - toxicity treatment

N-acetylecysteine

acetaminophen - adverse effects

skin rash, kidney disfunction, liver toxicity

most common inherited CT disorder

osteogenesis imperfecta

osteogenesis imperfecta - mutation

type 1 collagen gene

osteogenesis imperfecta - manifestations

blue, transparent sclera; fragile bone; hearing loss; abnormal teeth

what happens first in bone fracture healing

extensive blood clot in subperiosteum and marrow cavity

osteonecrosis (avascular necrosis) - what

death of bone and marrow without infection

osteonecrosis (avascular necrosis) - manifestations

pale and detached, empty structure without osteocyte

osteonecrosis (avascular necrosis) - cause

trauma, corticosteroid administration

osteoarthritis - what

degenerative joint disease

osteoarthritis - where

weight-bearing joints and finger of elderly

osteoarthritis - cause

degeneration of articular cartilage, inflammation

osteoarthritis - manifestations

osteophyte and narrowed joint space

rheumatoid arthritis - manifestations

pannus (synovium extensions into joint space), ankylosis (joint destruction), ulnar deviation

gout - what

inflammatory arthritis from urate crystals in joints

gout - where

big toe

gout - cause

excessive cell death (chemotherapy) leading to accumulation of uric acid

gout - manifestations

tophi

duchenne and becker muscular dystrophy - cause

loss of function mutation of dystrophin gene on x chromosome

duchenne muscular dystrophy

total absence of dystrophin

becker muscular dystrophy

retain some dystrophin

most common soft tissue tumor

lipoma

lipoma - what

benign neoplasm of adipocyte

components of dermis layer

ct, dense, fibrous, blood vessel, nerves

components of hypodermis

subcutaneous, ct

skin layer injections are injected into and why

hypodermis because fat absorbs well

functions of the skin

maintain homeostasis, site of Langerhans (APC), produce vitamin D

epidermis characteristics

keratinized stratified squamous, basement membrane, no vasculation

thick skin locations

palm, sole

what component is in thin skin that isn’t in thick skin

hair

epidermis layers starting from basement membrane

stratum basale, stratum spinosum, stratum granulosum, stratum lucidum, stratum corneum

cell types of epidermis

keratinocyte (majority), melanocyte, langerhans, merkel

what cell junction is present in stratum basale

hemidesmosome

stratum basale characteristics

single layer with mitosis (stem cell), keratinocytes rest on basement membrane

stratum spinosum characteristics

spikes from cell surface (prickle cells), langerhans

function of tonofibrils

bind to desmosome for cohesion and resistance to abrasion

stratum granulosum characteristics

keratohyalin granules (cysteine), lamellar granules (lipid coats), more purple

stratum lucidum characteristics

lack nucleus, only in thick skin, contain keratin filaments and eleidin

stratum corneum characteristics

lack nucleus, contain keratin, shed every 25 days

melanocyte location

stratum basale

dermal papilla

invaginations of dermis into epidermis

epidermal ridge

invaginations of epidermis into dermis

keratinocyte characteristics

originate from stratum basale, mitosis

melanocyte characteristics

originate from neural-crest cells, round nucleus with space around it, in basale, no desmosome

langerhans cell morphology

resemble melanocyte but in spinosum

melanin pigment formation

tyrosine > DOPA > dopaquinone > phenomelanin, eumelanin > transfer from melanocyte to keratinocyte

skin brightening mechanism blocks

tyrosinase

albinism

melanocytes can’t synthesize melanin

langerhans characteristics

found in all layers (especially spinosum), no desmosome

merkel (tactile) cells

derived from neural crest, found in stratum basale, in fingertips

carotene

yellow pigment from egg and vegetables

melanin accumulate where

keratinocytes of S. basale and S. spinosum

dermis characteristics

ct with fibers, contains glands and nerve endings

dermis layers and which is majority

papillary, reticular (majority)

papillary layer

loose ct, vascularized, dermal papillae

reticular layer

dense irregular ct, glycoaminoglycan for skin hydration

bullous pemphigoid

autoimmune blistering of dermis-epidermis junction

hypodermis

superficial fascia (subcutaneous), loose ct with adipose, contain sweat glands and hair

skin aging in epidermis, melanocytes, collagen and elastin, oil, subcutaneous fat, sweat

epidermis thinning but same number of cell layers, melanocytes increase in size but less amount, changes in collagen and elastin, less oil produced, thinner subcutaneous fat, less sweat produced