Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Unit 2: LGS > Week 5 > Flashcards

Week 5 Flashcards

1
Q

Gout -what is it

A

-caused by increase of UA levels which travel to joint and cause precipitation of crystals, which then causes inflammation in joint

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Gout -causes

A

-under excretion of UA -over production of UA -over production of UA with over excretion of UA but not enough

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Gout -test

A

-Serum uric acid level: check to see if UA is elevated in body -Urine uric acid level: check to see if UA is being under excreted–helps determine cause -Needle aspiration: look for crystals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Polarizing Light microscopy

A

-used to check for crystals in liquid from needle aspiration -crystals can be surrounding cells, or can be in macrophages/neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Gout arthritis

A

-erosion of bone joint due to inflammation caused by precipitation of monosodium uric crystals caused by excess UA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Why do crystals form in joints?

A

Articular joints are surrounded with synovial fluid, which has lower temperature and different viscosity in serum creating ideal place for crystal to precipitate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Gout classification -based on

A

-etiology -primary: unknown etiology; not caused by another disease process meaning that joint manifestation is primary -secondary: caused by another disease process

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Inflammatory process in gout -what causes more inflammation? -role of vasodilation -role of proteases

A

-Macrophage phago crystals–crystals recognized by inflammozone–release of capsone enzyme–release of pro-inflammatory cytokines (IL1 and TNF alpha)–neutrophils recruited–phago crystals then die and release crystals from lysosomes also releasing degradative enzymes–causes tissue damage and more inflammation -caused by cytokines, will induce erythema/edema/increase in temp -will damage cartilage in joint

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Risk factors of gout

A

-diet, obesity, diabetes -EtOH consumption-excessive -diuretic -genetic pre-disposition -male -drugs -duration–longer hyperuricemia the more likely you are to have gout

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Stages of gout (4)

A

-hyperurecemia: elevated uric acid -acute: inflammatory response due to elevation of uric acid -intercritical: asymptomatic but continue to have elevated levels or uric acid in serum -chronic tophaceous arthritis: inflammatory response comes back and can cause release of crytals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How is gout caused at cellular level?

A

Elevated levels of Uric Acid in body–linked to enzyme in charge or creating purines and pyrimidines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How are nitrogenous bases created?

A

-De novo pathway: brand new; made from scratch -Salvage pathway: Recover base and reuse–less energy–base is recovered from DNA mutations that are discovered during replication and translation and that are then fixed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How to make Purines DeNovo style

A

-start with Glutamine+PRPP (ribose-5-phosphate + ATP)+ATP -add glycine, glutamine (2), aspartate, 6 ATP, 2 formyl group, and CO2 forming IMP (Hyposanthine and a sugar) -To get adenine–add GTP and Aspartate to IMP making AMP; then add a phosphate (ADP); then use ribonucelotide reductase making dADP; then add another phosphate making dATP -To get glutamine–add ATP and glutamine to IMP; add a phosphate (GDP); then use ribonucleotide reductase to make dGDP; add another phosphate to make dGTP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How do purines lead to increase in Uric Acid

A

-Guanine can form xanthine with addition of NH4, and Xanthine is changed to uric acid with enzyme of xanthine oxidase -Adenine goes to AMP with loss of 2 phosphates, AMP forms IMP with loss of NH3, IMP forms inosine with loss of phosphate, Inosine forms hypoxanthine with loss of ribose1phosphate, Hypoxanthine can be transferred to xanthine with xanthine oxidase and xathine forms uric acid with xanthine oxidase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

HGPRT

A

-Deficiency of HGPRT will lead to over accumulation of guanine and hypoxanthine–causing hyper-urecemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Types of HGPRT deficiency

A

-Quantitative: 20% or less -Severe/total: Lesch Nyhan Syndrome- juvenile gout

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Xanthine oxidase inhibition -rationale

A

Will prevent purine from being converted to xanthine, which will then not be converted to uric acid–lower uric acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

MOA of xanthine inhibition -allopurinol

A
  • isomer of hypoxanthine–which will make oxypurinol by xanthine oxidase to competitively inhibit binding of xanthine oxidase to xanthine and hypoxanthine– which prevents uric acid from being made - Febuxostat: alternative xanthine oxidase inhibitor that binds to xanthine oxidase which will render the enzyme ineffective–allosteric modifier
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

MOA of xanthine inhibition -fubuxostat

A

binds to xanthine oxidase which will render the enzyme ineffective–allosteric modifier

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Therapeutic goal for treatment of gout

A

-reduce SUA level to less than 6.0 mg/dL (levels above 6.8 mg will cause precipitation of crystals)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Purines-Salvage style

A

-Adenine can be broken down into Hypoxanthine which is then broken down into IMP which can be turned into GMP and then turned into Guanine -Hypoxanthine can be used to make adenosine through use of HGPRT which breaks hypoxanthine down to IMP–to AMP–to adenosine -Guanine can be broken down into GMP to make HGPRT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Difference between catabolism of purines and pyrimidines

A

-purines will be made into uric acid and excreted in urine while pyrimidines will be broken down into alanine (cysteine–can be used to make pyruvate) and aminoisobutyrate (tyrosine–later converted to TCA cycle intermediates) which eventually leads to ATP production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Occurence in fractures -vs other dx -old vs young -women vs men

A

-Fractures occur more often than the leading causes of death in the US (heart attack, stroke, breast cancer) -The increase in prevalence of a fracture increases with age -Men have a spike in their chance to get a fracture when young (testosterone syndrome) but women have higher chance of fracture when older due to loss of estrogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Types of fractures

A

-Simple -Comminuted -Stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Simple fracture

A

bending force or twisting force is applied to a bone, resulting in two fragments with transverse, oblique or long curved (spiral) edges of the broken bones. This type of fracture heals through the spontaneous repair

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Comminuted fracture

A

breaking of a bone into several small pieces and is the result of high velocity injuries, like car accidents, or falls from a height. Repair of comminuted fractures follows a healing pattern similar to that of simple fractures, but on a larger scale. Such fractures generally are very difficult to treat, and may result in a deformity of the injured part even after treatment.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Stress fracture

A

overuse injury, results from repetitive loading–minor injuries to the bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Stages of healing

A

1: Inflammatory response 2: Soft callus formation 3: Hard callus formation 4: Bone remodeling

29
Q

Inflammatory Response

A

-vascular supply of bone is disrupted and a hematoma forms at the site of the injury–causes a lack of local oxygen and nutrients, and a release of various factors from platelets. -Macrophages, leukocytes, and other inflammatory cells then invade the area. This inflammatory response peaks within the first 24 h and lasts for about 7 days.

30
Q

Soft Callus Formation (Cartilage Formation)

A

-The cells that are stimulated and sensitized during the inflammatory stage begin producing new vessels, fibroblasts, intracellular material, and supporting cells. The hematoma is replaced with fibrovascular tissue, a fibrin-rich granulation tissue. Fibrocartilage then develops and stabilizes the bone ends

31
Q

Hard Callus Formation (Endochondral Ossification) -cartilage -peripheral site

A

-replacement of the cartilage and fibrovascular tissue occurs via vessel invasion and endochondral ossification. -Periosteal bone apposition also occurs, contributing to formation of the hard callus. -The calcified cartilage is replaced with woven bone. -Intramembranous ossification peripheral to the site of the fracture also contributes to the hard callus for structural support

32
Q

Bone Remodeling -woven bone -hard callus -ischemic bone tissue

A

-woven bone is gradually replaced by lamellar bone via bone remodeling (see Chapter 4). -Hard callus resorption by osteoclasts is followed by lamellar bone formation by osteoblasts to restore the anatomical structure of the pre-injured bone and support mechanical loads. -The ischemic bone tissue (the original cortex) at the fracture site is resorbed as the outer cortical shell remodels inward to become the new diaphyseal bone. Osteoclasts carry out two tasks during fracture healing: removal of endochondral matrix and remodeling of woven bone.

33
Q

Prostaglandins and bone healing -effect on healing -mechanism

A

-increase healing -made from arachadonic acid and cox 2; cause increase in vascularity of fracture site

34
Q

NSAIDS and bone healing -effect on healing -mechanism

A

-decrease -decreased inflammatory phase response

35
Q

BMPS and bone healing -effect on healing -mechanism

A

-increase -increase proliferation and differentiation of chondrocytes and osteoblasts

36
Q

VEGF and bone healing -effect on healing -mechanism

A

-increase -increase angiogenesis

37
Q

Aging and bone healing -effect on healing -mechanism

A

-young: increase; old: decrease -ability of cell to heal quickly–cell deterioration with increase in age

38
Q

Diabetes and bone healing -effect on healing -mechanism

A

-decrease -T1: decrease in insulin=decrease in formation of bone; T2: increase glucose=decrease in proliferation and function of osteoblasts

39
Q

EtOH and bone healing -effect on healing -mechanism

A

-decrease -decrease osteoblast proliferation and differentiation

40
Q

Glucocorticoids and bone healing -effect on healing -mechanism

A

-decrease -decrease in osteoblast and chondrocyte proliferation; increase in osteoblast apoptosis

41
Q

PTH and bone healing -effect on healing -mechanism

A

-increase -increases proliferation of osteoblasts, delayed apoptosis of osteoblasts and chondrocytes

42
Q

Bisphosphonates and bone healing -effect on healing -mechanism

A

-decrease -inhibit osteoclast resorption – impairs removal of damaged bone

43
Q

Name of growth plate

A

physis

44
Q

Types of Fractures

A

-Transverse -Linear -Oblique, nondisplaced -Oblique, displaced -Spiral -Greenstick -Comminuted

45
Q

Special Fractures

A

A: impacted B: avulsion C: compression fracture D: pathological fracture- result in flaw of bone

46
Q

-What kind of fracture is this? -What type of patient is it seen in? -Describe each type

A
  • Salter Harris
  • Child
  • Type I: right through growth plate, does not show up well on conventional x-ray; Type II: proximal and growth plate; Type III: distal and growth plate; Type IV: proximal and distal + growth plate; Type V: crush of growth plate
47
Q

What kind of injury is this? Common cause?

A
  • Fight bite
  • Patient punches someone in jaw and is cut by their teeth
  • Skin being broken by teeth makes this open fracture and allows for possibility of infection
48
Q

What kind of fracture is this? Common cause?

A
  • Boxer fracture: 5th metacarpal dislocation
  • Not knowing how to punch
49
Q

What is apposition?

A

-Amount that bone has been horizontally displaced due to a fracture

50
Q

What is distraction?

A

-Gap between 2 ends of a bone caused by fracture

51
Q

What kind of fracture is this? Cause?

A
  • Avulsion
  • Cause by ligament tearing and pulling bone
52
Q

What does it mean when a fracture bayonetes?

A

two ends of bone overlap

53
Q

Smith vs Choles fracture

A

angulated fracture to distal radius -smith: apex is to volar side of arm -choles: apex is to dorsal side of arm

54
Q

What occurs when a fracture is impacted?

A

Bone fractures and one end is crushed into the other

55
Q

What kind of fracture is this? Commonly seen in? Cause?

A
  • Buckle fracture
  • children
  • side of the bone under compression crunches down upon itself causing the bone to crumple on just the one side of the bone.
56
Q

How does acetaminophen eliminate pain?

A
  • analgesic-may have some effect on COX but only see in lab
  • may have effect on inhibitory pathway controlling pain
57
Q

Clinical Presentation of osteoarthritis in hands

A
  • hypertrophy seen in Distal interphalangeal and Proximal interphalangeal joint
  • Carpo-metacarpal (thumb) joint would also be affected
  • hands would feel hard
58
Q

Clinical presentation of rheumatoid arthritis vs osteoarthritis

A
  • classically affect metacarpal phalangeal proximal interphalangeal joint (NOT DIP joints)
  • would also be boggy/swelling instead of hard
59
Q

Histopathology of Osteoarthritis

A
  • Bony hypertrophy
  • Narrowed joint space
  • Increase in amount of cartilage cells
  • May also see horizontal or deep vertical fraying with advanced tissue damage
60
Q

Treatment for osteoarthritis of hand

A

-NSAIDS: Cox inhibitors which has analgesic and anti-inflammatory response; 1st line is topical (especially with kindey disease)

61
Q

Why can’t we use NSAIDS with elevated creatine and low GFR?

A
  • Indicative of kidney disease
  • COX2 is used to help with dilation of blood vessels in kidneys to help with moving the blood through and making filtration easier
  • NSAIDS would inhibit COX2 causing vasoconstriction making it harder for kidneys to filtrate and thus worsening the disease
62
Q

Tramadol

  • used for
  • how does it work
  • down side
A
  • can be used as analgesic for pain
  • binds to mu, sert, and nor adrenergic pre-synaptic neurons and prevent re-uptake of nor-epi and serotonin which allows them to continue their inhibition on post-synaptic cells, preventing action potential caused by pain from spreading
  • if tramadol effects are too much, they are hard to reverse because the medication used, naloxone, can only bind to one of the three receptors that tramadol binds to making it a partial antagonizer of tramadol
63
Q

Gluco-corticoid MOA for injections

A

-represses transcription of pro-inflammatory cytokines

-

64
Q

Gluco-corticoid pathway

A

-steroid binds to corticoid-binding globulin; then steroid diffuse into the cell; binds to chaperone proteins; dimerization of steroids occurs; goes into nucles; binds to GRE (glucocorticoid response element) and regulates transcription by either increasing or decreasing

65
Q

Duloxetine

-how it effects pain

A

-serotonin re-uptake inhibitor

66
Q

Celecoxib

-MOA

A

-Cox 2 inhibitor

67
Q

Central sensitization

A

Body becomes sensitized to nocireceptive neurons due to constant stimulation from inflammation which causes the CNS to reduce inhibition. This then allows the threshold for action potential to be conducted to lower, which allows for CNS to receive more and more information which makes it feel like there is more pain

68
Q

Treatment of osteoarthritis in knee

-medication and MOA

A
  • Duloxetine (SNRI): Increase nor-epi in synapse to inhibit excitatory action that is delivering pain; also helps with depression
  • Gabapentin: Inhibit enzyme that allows for opening of voltage gated Ca channels which prevents the calcium from going into nerve and having glutamine released; Anti-seizure drug

Unit 2: LGS (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions