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PBL SEM 1 > CASE 8 (includes some pharm) > Flashcards

CASE 8 (includes some pharm) Flashcards

1
Q

what is osteoporosis?

A

a disease characterised by low bone mass (decreased bone mineral density BMD) and micro-architectual degeneration of bone tissue, leading to enhanced bone fragility and an increase in fracture risk

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2
Q

according to WHO, in osteoporosis the BMD is what below a normal healthy age-matched control?

A

BMD < 2.5 standard deviations a below a normal healthy age-matched control

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3
Q

what is T score?

A

patient’s BMD compared to young healthy control

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4
Q

what is Z score?

A

patient’s BMD compared to age-matched control

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5
Q

what is osteopenia?

A

defined as between 2.5 and 1 standard deviation below normal heathy control — can go on to develop osteoporosis

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6
Q

osteoporosis affects who?

A
  • affects 1/3 of all UK women

- affects 1/12 of all UK men

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7
Q

what is the cost of osteoporosis to the NHS each year?

A

over £3 billion a year

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8
Q

name key differences between bone in an 18 year old vs. an 80 year old

A

18 year old — epiphyseal plate still open, trabeculae, relatively thick cortices of bone

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9
Q

what is the effect of menopause on osteoclasts?

A

increases the number of osteoclasts

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10
Q

what is the effect of menopause on osteoblasts?

A

decreases the number of osteoblasts

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11
Q

what are the falling oestrogen levels in menopause associated with? effect of osteoporosis?

A

increased osteoclasts associated with falling oestrogen levels. however bone secretions from women with osteoporosis show problems with osteoblasts therefore fewer esteoclasts

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12
Q

why is there a deficit in BMD?

A
  • osteoblasts simply no longer “catch up” with the activity of osteoclasts — lower BMD
  • menopause, with relatively sudden increase in osteoclast activity accelerates this process
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13
Q

what are the actions of oestrogen on osteoblasts?

A
  • increased alkaline phosphatase expression
  • increased collagen type 1 synthesis
  • stimulates growth factors synthesis (IGF1, TGF-B, BMPs) — all important for controlling cell division and differentiation
  • regulates osteoblast proliferation
  • stimulates expression of VDR, marker for osteoblast maturation
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14
Q

what are the actions of oestrogen on osteoclasts?

A
  • increases apoptosis of osteoclasts
  • suppresses osteoclast differentiation
  • act on osteoclasts via osteoblasts (IL6 or RANK/RANKL, osteoprotegerin)
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15
Q

where are RANK receptors located?

A

on the surface membrane of osteoclast progenitor cells

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16
Q

what is RANKL?

A

rank ligand that binds to RANK receptor in osteoclast activation

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17
Q

what secretes RANKL?

A

osteoblasts

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18
Q

what is the effect of RANKL binding to the RANK receptor?

A

initiates intracellular signalling and gene expression cascade that results in differentiation and maturation of the precursor cells into osteoclasts

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19
Q

what does osteoprotegerin do?

A

OPG protects the skeleton from excessive bone resorption by binding to RANKL and preventing it from binding to RANK receptor

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20
Q

what promotes the synthesis of OPG (osteoprotegerin)

A

oestrogen

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21
Q

what is the overexprexssion of RANKL linked to?

A

osteoporosis

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22
Q

what bone markers are used for osteoblasts and osteoclasts?

A
  • osteoblasts = alkaline phosphatase

- osteoclasts = collagen breakdown products (teleopeptides)

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23
Q

what is osteoporosis a disease of?

A

bone remodelling

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24
Q

how long does 1 bone remodelling cycle take?

A

around 9 months

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25
Q

why is a biochemistry test for osteoporosis disappointing?

A

in a biochemistry test in a blood sample, the cellular markers will be diluted out and will not change significantly enough to indicate that a disease process is ongoing

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26
Q

is there a higher morbidity and mortality in men or women with osteoporosis?

A

men

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27
Q

risk factors for osteoporosis

A
  • oestrogen deficiency
  • vitamin D insufficiency
  • hypocalcaemia (diet or hypoparathyrodism)
  • increasing age
  • sedentary lifestyle
  • asian descent
  • family history
  • long term use of corticosteroid medications (eg. prednisolone)
  • excessive alcohol consumption
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28
Q

why is osteoporosis less common in men than in women?

A

because men have a higher ‘peak bone mass’ than women

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29
Q

what is corticosteroid therapy used for?

A
  • asthma (inhaled and oral formulations)
  • rheumatoid arthritis
  • other autoimmune diseases (SLE)
  • inflammatory diseases (Chron’s Disease)
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30
Q

what is the most abundant mineral in the human body?

A

calcium

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31
Q

what is the normal range of Ca conc in the blood and what is said to be average?

A

normal = 9-10.5 mg/dl or 2.2-2.6 Mmol/L

average = 9.4 mg/dl

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32
Q

how is calcium present in the bones?

A

present as calcium phosphate

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33
Q

what hormones controls calcium homeostasis?

A

parathyroid hormone — increases Ca

calcitonin — decreases Ca

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34
Q

where are parathyroid hormone and calcitonin produced?

A

parathyroid — parathyroid gland

calcitonin — follicular cells in the thyroid gland

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35
Q

factors that increase calcium levels

A
  1. parathyroid hormone causes the kidneys to retain Ca ions
  2. parathyroid hormone (with calcitriol) causes the rate of intestinal absorption to increase
  3. osteoclasts are stimulated to release stored Ca ions from the bone
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36
Q

factors that decrease calcium levels

A
  1. calcitonin causes kidneys to allow calcium loss
  2. calcitonin doesn’t have a direct effect on the rate of absorption
  3. decreased parathyroid hormone (or calcitriol) causes a decrease in the rate of intestinal absorption
  4. osteoclasts are inhibited whilst osteoblasts continue to lock Ca ions in the bone matrix
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37
Q

what do melanosomes in the skin do?

A

convert a precursor into cholecalciferol (inactive vitamin D3)

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38
Q

what happens to the cholecalciferol?

A

it is hydroxylated to calcifediol/calcidiol (25-hydroxyvitamin D3) in the liver

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39
Q

what happens to the calcifediol/calcidiol?

A

it is hydroxylated to calcitriol/calciferol (1,25-dihydroxyvitamin D3) = ACTIVE FORM OF VITAMIN D3 in the kidney

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40
Q

what does calcitriol do?

A

it increases calcium absorption in the small intestines, kidneys and bones

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41
Q

what else does the activation of calcitriol lead to in the intestines?

A

leads to the formation of calbindin, a calcium binding protein in the intestinal epithelial cells, which transports calcium into the cell cytoplasm

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42
Q

what is the effect of long term corticosteroids on Ca?

A
  • shuts of Ca resorption through the gut

- stops the 1,25-dihydroxyvitamin D3 having its action on the intestine

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43
Q

what do corticosteroids act on in the bone and what is their effect?

A

osteoblasts — decrease osteoblast activity (collagen type 1) and possibly osteoblast number.

(complex pathway of osteoblast differentiation from mesenchymal stem cells, in which osteoblasts themselves may have a role — some of this is corticosteroid dependent)

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44
Q

treatment for osteoporosis

A
  1. HRT for women with osteoporosis — however bad side effects such as breast cancer so no longer really used
  2. bisphosphonates (compounds related to bone phosphate, decrease osteoclast activity) — latest developments are IV administration (zolendronic acid once per year and residonate) — but newly recognised side effects of osteonecrosis of the jaw and NOT tolerated in oral formulation by some patients
    - SERMs (Selective Estrogen Receptor Modulators, like raloxifene, tissue specific)
    - calcium, vit D supplementation
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45
Q

what is menopause? how is it clinically defined?

A

= the permanent cessation of menstruation that results from the loss of ovarian follicular activity

  • clinically defined as when a woman has not had a period for 12 consecutive months
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46
Q

when does menopause typically occur and what is the mean age?

A

occurs 45–55 years, mean = 51 years

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47
Q

what is peri-menopause and what happens here?

A

= time leading to menopause

  • there is an increase in oestrogen, leading to peak bone mass
  • oestrogen levels begin to decline after this surge of oestrogen due to a decrease in ovarian follicles
  • this surge in oestrogen prepares the body for the effects of post menopause
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48
Q

what is post-menopause and what happens here?

A

= the time after menopause

- there is a very high level of FSH, due to decreased levels of oestrogen

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49
Q

what are 2 possible effects of the decreased oestrogen?

A
  • CHD because of increased production of LDL in the liver

- osteoporosis

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50
Q

what are the primary causes of premature menopause?

A
  • chromosomal abnormalities (40%)
  • autoimmune disease
  • insufficient oestrogen synthesis
  • metabolic disorders
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51
Q

what are the secondary causes of premature menopause?

A
  • radiotherapy
  • surgery
  • hysterectomy
  • infection — TB, mumps
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52
Q

what are some symptoms of menopause?

A
  • hot flushes (night sweats)
  • changes in period (irregular)
  • abnormal bleeding (spotting)
  • emotional changes (mood swings, anxiety)
  • vaginal changes (dry and thin)
  • urinary incontinence
  • decrease in sexual drive
  • weight gain/gain in body fat
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53
Q

what is HRT?

A

= hormonal replacement therapy

  • possible treatment to menopause
  • women with intact uterus — oestrogen + progesterone
  • women after hysterectomy — oestrogen
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54
Q

what is the most likely cancer caused by oestrogen?

A

womb cancer

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55
Q

HRT routes — oestrogen

A
  1. transdermal — patch or gel — local skin irritation

2. oral oestrogen — cost effective, acceptable route

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56
Q

HRT routes — vaginal oestrogen

A
  1. cream, tablets or vaginal rings
  2. local delivery

urogenital symptoms — dryness, painful intercourse

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57
Q

HRT routes — progesterone

A
  1. micronised progesterone
  2. oral derivatives
  3. mineral coil — progesterone released intrauterine coil
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58
Q

use of testosterone supplementation?

A

used for low sexual drive, if HRT alone is not effective

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59
Q

name some risks of HRT

A
  • breast cancer
  • stroke
  • venous thromboembolism
  • ovarian cancer
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60
Q

HRT after breast and cervical cancer?

A

breast — avoid systemic HRT. can use topical oestrogen, consider clonidine or paroxetine

cervical — if young, ovarian conservation recommended. systemic HRT can be used

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61
Q

HRT after endometrial and ovarian cancer?

A

endometrial cancer — if stage 1, can consider ovarian conservation or HRT. if later stage, HRT usually contradicted

ovarian cancer — HRT not usually contradicted, unless tumour has oestrogen receptors

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62
Q

what are 3 types of fractures?

A
  1. external appearance (open/closed)
  2. location (compression/epiphyseal)
  3. nature of crack or break (incomplete/complete, linear/transverse)
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63
Q

what is a colles fracture?

A

a break of the distal portion of the radius, and is typically the result of reaching out to cushion a fall

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64
Q

what are the 2 types of treatment for a fracture?

A

1) surgical

2) conservative : pain relief, immobilisation, stabilisation (all non-surgical)

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65
Q

what are some risk factors for fractures?

A
  • previous fracture
  • increasing age
  • long term glucocorticoid therapy
  • smoking
  • falls
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66
Q

how does long term glucocorticoid therapy increase the risk of a fracture?

A

corticosteroids reduce Ca resorption and decrease osteoblast activity

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67
Q

describe kyphosis and what it may result from

A

= an exaggerated thoracic curve

  • it is a condition of over-curvature of the thoracic vertebrae where it has lost its lordotic profile (inward curvature)
  • result from degenerative diseases (such as arthritis). developmental problems, osteoporosis with compression fractures of the vertebrae, or trauma
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68
Q

treatment options for kyphosis

A
  • brace
  • specialised physical therapy
  • surgery
69
Q

what are the 3 phases of wound healing?

A

1) inflammatory phase
2) proliferation phase
3) maturation phase

70
Q

what happens in the inflammatory phase of wound healing?

A
  • blood clot forms
  • haemostasis (the stopping of bleeding) occurs to allow for vascular dilation to initiate inflammation
  • leads to a rise in exudate levels
  • the surrounding skin needs to be monitored for signs of maceration (a softening or wetting of the skin owing to retention of excessive moisture
71
Q

what is exudate?

A

a mass of cells and fluid that has seeped out of blood vessles

72
Q

what happens in the proliferation phase of wound healing?

A

wound ‘rebuilt’ with new granulation tissue

73
Q

what is granulation tissue?

A

connective tissue (collagen + extracellular matrix) and blood vessels

74
Q

what is healthy granulation tissue like and when does it occur?

A
  • occurs when fibroblasts receive sufficient levels of oxygen and nutrients supplied by the blood cells
  • it is granular and uneven
  • it doesn’t bleed easily
  • pink/red in colour
75
Q

what are fibroblasts?

A

the most common type of cell found in connective tissue — secrete collagen

76
Q

what is used as an indicator of how the wound is healing?

A

the colour and condition of granulation tissue

- dark granulation tissue = poor perfusion/ischemia and/or infection

77
Q

what is epithelialisation?

A

when epithelial cells finally resurface the wound

78
Q

what happens in the maturation phase of wound healing?

A
  • occurs once the wound has closed
  • this phase involved remodelling of collagen type III to type I
  • cellular activity reduces and the number of blood vessels in the wounded area decreases
79
Q

what is SIRS?

A

Systemic Inflammatory Response Syndrome

80
Q

what is sepsis?

A

SIRS triggered by a primary localised infection

81
Q

what are the symptoms of SIRS and sepsis?

A

2 or more of:

1) temp of <36 or >38
2) tachycardia = HR > 90bpm
3) resp rate > 20 per min OR PaCO2 < 4.3 kPa
4) white cell count > 12 x 109/L OR < 4 x 109/L

sepsis = 2 or more of these resulting from an infection

82
Q

what is severe sepsis?

A

sepsis along with signs of organ hypo-perfusion. signs include hypoxemia, oliguira, lactic acidosis or acute alteration in mental state

83
Q

what is septic shock?

A

severe sepsis with hypotension (systolic BP < 90 mmHg or a decrease of > 40 mmHg from baseline OR the requirement for vasoactive drugs — despite adequate fluid resuscitation

84
Q

potential sites of infection causing sepsis in a healthy adult (+ an example of organism)

A
  1. skin — staphylococcus aureus
  2. respiratory tract — streptococcus pneuomoniae
  3. gall bladder/bowel — Escherichia coli, enterococcus faecalis
  4. pelvic viscera — Neisseria gonorrhoeae
85
Q

what is prednisolone?

A

= glucocorticoid

  • used to treat: autoimmune conditions, hypersensitivity and inflammation
  • it suppresses the immune system by restraining the clonal expansion of Th cells (decreasing transcription of the gene for Il-2), thus leaving the patient susceptible to infection
  • long term use of this can lead to osteoporosis
86
Q

what is bendrofluazide/bendroflumethiazide?

A
  • drug that reduces the uptake of water
  • blocks the Na/K pumps that would allow uptake of Na and K ions and hence water in the ascending arm of the Loop of Henle (from the renal filtrate into the blood)
  • used to treat hypertension (high blood pressure ) and oedema (water retention)
  • reducing the amount of excess water reduces the work of the heart
87
Q

what is co-codamol?

A
  • compound analgesic consisting of a combination of codeine phosphate and paracetamol
  • co-codamol tablets are used for the relief of mild to moderate pain when paracetamol alone does not sufficiently relieve a patient’s symptoms
88
Q

what is codine?

A
  • acts as a prodrug — metabolised to morphine
  • effective only in mild pain
  • it blocks transmission of pain signals sent by nerves to the brain
89
Q

what is paracetamol?

A
  • analgesic (pain relief)
  • acute overdose can cause potentially fatal liver damage
  • active ingredient in many flu medications
90
Q

what is diazepam?

A
  • used to treat: anxiety, insomnia
  • increases the activity of GABA in the brain
  • GABA is a neurotransmitter that acts as a natural ‘nerve-calming’ agent
  • it helps keep the nerve activity in the brain in balance, and is involved in inducing sleepiness, reducing anxiety and relaxing muscles
  • not supposed to be prescribed for more than 4 weeks at a time
91
Q

what are the principle molecules in the development of sepsis?

A

CYTOKINES - eg. interleukins (eg. IL-b), TNF-a, TGF-b

92
Q

infection control

A

1) prevention of transfer from source to patient — contact precautions (clean hands/equipment/environment), recognition and isolation of infected patients
2) minimise skin disruption/breaching — surgical and aseptic techniques, prevention of pressure ulcers/skin tears/macerated skin
3) treatment — surgical (correct incisions and drainage), foreign body removal, antibiotics

93
Q

how to penicillins work?

A
  • penicillin/methicillin attach via their B-lactam ring (which opens up) to the target in the cell wall (Penicillin Binding Protein PBP)
  • this changes the functional group of the PBP
  • as the cell wall grows, it is weakened and crumbles.
  • extracellular fluid enters causing lysis
94
Q

what is the bacterial response to penicillin?

A

bacteria produce the enzyme B-lactamase which breaks down B-lactam ring medication (penicillin/methicillin) so they are no longer effective

95
Q

how to bacteria respond to flucloxacillin?

A

bacteria changes shape of the binding protien so the medication is no longer effective

96
Q

what drug is able to bind to the modified PBP?

A

vancomycin

97
Q

what are staphylococcus aureus not resistant to?

A

vancomycin

98
Q

what are some effects of aging?

A

1) musculoskeletal — decreased BMD = osteoporosis
2) endocrine — female menopause, decreased GH and adrenal hormones (corticoids and adrenaline)
3) Ca metabolism decreases
4) cardiovascular — arteries develop atherosclerotic change
5) GI system —liver loses cells and blood flow
6) renal system — kidneys shrink and reduced blood flow

99
Q

what is frailty?

A

refers to a person’s mental and physical resilience or their ability to bounce back and recover from events like illness and injury

100
Q

how do you treat infections?

A
  • symptomatically (viral infections)
  • topically (superficial infections)
  • by removing the focus of the infection
  • surgically (abscesses, biofilms)
  • immunotherapies (antibodies)
  • by prescribing antimicrobials
101
Q

what are the 10 main categories of antibiotics?

A
  1. betalactams
  2. tetracyclines
  3. macrolides
  4. clindamycin
  5. quinolones
  6. sulfonamides
  7. aminoglycosides
  8. glycopeptides
  9. nitrofurans
  10. metronidazole
102
Q

what are the 2 types of antibiotic therapy?

A
  1. empiric therapy

2. targeted therapy

103
Q

describe empiric therapy

A
  • initiation of treatment as per guideline PRIOR TO DETERMINATION OF A FIRM DIAGNOSIS
  • typically broad-spectrum (covers all relevant bacteria)
104
Q

describe targeted therapy

A
  • targeted at microorganisms proven to be causing disease

- initiate when culture report is available or change from empiric to targeted

105
Q

what are 3 indications for using antibiotics?

A
  1. therapy — use of antibiotics in the treatment of infection
  2. pre-emptive therapy — use of antibiotics in the treatment of presumed infection
  3. prophylaxis — use of antibiotics to prevent the development of an infection
106
Q

ON EXAM DONT SAY RESISTANCE IS DUE TO OVER USE OF ANTIBIOTICS

A

hello

107
Q

what are common signs of infection?

A
  • redness
  • swelling
  • heat
  • pain
  • loss of function
  • fever
  • fatigue
  • night sweats
  • necrosis
  • headache
  • respiratory symptoms
  • weight loss
  • rash
108
Q

when must empiric therapy be used?

A
  • when the consequences of treatment delay are a serious deterioration in condition
  • when diagnostic tests are slow or samples are difficult to obtain
109
Q

what are 5 antibiotics with potential significant drug-drug interactions?

A
  • rifampicin
  • macrolides (clarithromycin)
  • ciprofloxacin
  • metronidazole
  • azole antifungals (itraconazole)
110
Q

describe staphylococci

A
  • gram positive cocci in groups
  • facultative anaerobes (can survive in and out of oxygen)
  • classified according to ability to coagulate serum
  • staphylococcus aureus (coagulate positive) is the main pathogen
  • coagulase-negative staphylococci (CNS) are less pathogenic
  • resistance is common among CNS
  • form biofilms rapidly and are a common finding in medical device associated infections
111
Q

what does S. aureus cause?

A
  • superficial skin lesions (impetigo, styles) and localised abscesses
  • deep-seated infections such as pneumonia, osteomyelitis and and endocarditis and more serious skin infections
  • a major cause of hospital acquired infections of surgical wounds
  • food poisoning by releasing toxins into food
  • toxic shock syndrome by releasing toxins into the blood stream
112
Q

S. aureus vs. Streptococcus

A

S. aureus are gram-positive cocci and from clusters. Streptococcus are gram-positive cocci and form chains

113
Q

what are the main mechanisms of antibiotic resistance?

A
  1. chemically modify the antibiotic (penicillases, betalactamases, carbapenemases)
  2. render it inactive through physical removal from the cell (efflux pumps)
  3. modify the target site so that it is not recognised by the antibiotic
114
Q

describe MRSA and what it is

A

MRSA = Methicillin Resistant Staphylococcus aureus
= a bacterium that causes infections in different parts of the body
- spread by contact
- carried by about 2% of the population

115
Q

why is MRSA tougher to treat than most staph strains?

A

it is resistant to some commonly used antibiotics

116
Q

what does MRSA typically cause?

A
  • most often it causes mild infections on the skin, like sores, boils or abscesses
  • can also be more serious and cause serious skin infections or infect surgical wounds, the bloodstream, the lungs or the urinary tract
117
Q

who are MRSA infections common in?

A

people with a weak immune system who are in hospitals, nursing homes, and other health care centres

118
Q

what is MRSA resistant to?

A

methicillin, penicillin, amoxicillin, oxacillin, and other common antibiotics known as cephalosporins

119
Q

where do MRSA infections typically appear?

A

around surgical wounds or invasive devices, such as catheters or implanted feeding tubes

120
Q

what is CA-MRSA and why is it a problem?

A

= community-acquired MRSA

  • MRSA is now also showing up in healthy people who have not been hospitalised
  • more likely to affect young people
121
Q

treatment of an MRSA infection

A

there are antibiotics available that can kill MRSA germs. some types of MRSA infections need surgery to drain infected areas. often required to consult a microbiologist

122
Q

describe the gram stain

A
  • cells fixed onto a microscope slide and a dye (‘stain’) is added
  • this reveals bacterial morphology eg. capsules, endospores, flagella
  • differentiates bacteria into gram positive and gram negative
  • test also reveals the shape of each bacterial cell
123
Q

gram positive vs. gram negative bacteria

A

gram-positive — thicker peptidoglycan layer, 2 layer structure

gram-negative — have an outer membrane composed of lipopolysaccharide, phospholipids and proteins, 3 layer cell wall

124
Q

how is a gram stain carried out?

A
  1. cells are fixed to a microscope slides
  2. stained with a purple dye - CRYSTAL VIOLET
  3. all bacteria cells stain purple
  4. addition of iodine allows large crystal complexes of crystal violet-iodine to form that become enmeshed in the peptidoglycan layer of the bacterial cells
  5. acetone is then added — dissolves lipids in the outer membrane of the cells that have one — dye crystals removed from the thinner peptidoglycan layer — leaves these bacteria colourless, whereas other bacteria remain purple
  6. a red counter stain is added - RED SAFRANIN
  7. the decoloured bacteria stain red
125
Q

which bacteria cells become red and which stay purple?

A

purple bacteria = GRAM POSITIVE

red bacteria = GRAM NEGATIVE

126
Q

what is pharmacokinetics?

A

what your body does to the drug

127
Q

what is pharmacodynamics?

A

what the drug does to your body

128
Q

what 4 things does pharmacokinetics include?

A
  • absorption
  • distribution
  • metabolism
  • excretion
129
Q

changes to pharmacokinetics due to ageing — absorption

A
  • some reduction in secretion of gastric acid and enzymes in GI tract
  • reduced total SA
  • some slowing of gastric emptying/motility
  • potential decrease in absorption of drugs
  • overall SMALL CHANGE
130
Q

changes to pharmacokinetics due to ageing — distribution

A
  • lower muscle mass
  • lower total body water
  • higher body fat
  • overall BIG CHANGE
131
Q

lipid-soluble vs. water-soluble drug distribution change with ageing

A

1) LIPID-SOLUBLE — greater volume of distribution, can gradually accumulate in fat and brain tissue, effects prolonged
2) WATER-SOLUBLE — smaller volume of distribution, can lead to higher serum levels, toxicity if drug has a narrow therapeutic index

132
Q

changes to pharmacokinetics due to ageing — metabolism

A
  • lower hepatic volume and blood flow (40%)
  • lower first pass metabolism
  • higher bioavailability of some drugs metabolised by the liver
  • smoking, alcohol co-existing disease and some drugs can impair liver function
  • overall SMALL CHANGE
133
Q

changes to pharmacokinetics due to ageing — excretion

A
  • renal function reduces with age
  • also reduced by coexisting chronic conditions eg. diabetes, CF and acute illness such as UTI and dehydration (common in elderly people)
  • reduced clearance of drugs which are excreted via filtration at the kidney (eg. digoxin) or actively secreted by the renal tubules (eg. penicillin)
  • can result in drug and metabolite accumulation and toxicity — therefore may need a dose-reduction
  • overall BIG CHANGE
134
Q

what is polypharmacy?

A

the use of multiple medications by a patient (usually 5+)

135
Q

what does increasing the number of drugs prescribed increase the risk of?

A
  • adverse drug reactions (ADRs) / side effects
  • drug-drug interactions
  • older patients more susceptible to ADRs and interaction due to changes in pharmacokinetics and changes in pharmacodynamics (increases sensitivity)
136
Q

describe prescribing cascades

A
  • where a new drug is prescribed to treat an unrecognised ADR or symptoms of a drug-drug interaction between existing medications
  • ADRs misdiagnosed as new medical conditions
  • contribute to polypharmacy
137
Q

what are the effects of ADRs on patients?

A
  • unnecessary investigations, treatment delays
  • longer hospital stays
  • negative impact on quality of life
138
Q

what is the impact of polypharmacy in older patients?

A
  • increasing the number of medications can lead to problems with ADHERANCE
  • aggravated by visual and cognitive impairment
  • leads to increased dependence on others
139
Q

how can polypharmacy be prevented?

A
  • only prescribe if necessary and patient in agreement
  • consider:
    1. numbers needed to treat (NNT) vs. harm (NNH)
    2. review medications regularly
    3. use tools to help medication review
140
Q

what is NNT?

A

= Numbers Needed to Treat
= the average number of patients who need to be treated to prevent one additional bad outcome

eg. reduction from 50-40% = 0.5-0.4 = 0.1

1/0.1 = 10

perfect number = 1

141
Q

what is NNH?

A

= Numbers Needed to Harm
= how many patients on average need to be exposed to a risk-factor over a specific period to cause harm in one patient who would otherwise not have been harmed

142
Q

how can medicines be optimised?

A

MEDICINES OPTIMISATION = a person-centred approach to safe and effective medicines use, to ensure people obtain the best possible outcomes from their medicines

  • sensible prescribing practice
  • is it an iatrogenic illness (caused by existing medical treatment)
  • consider non-pharmacological approaches
  • use a limited formulary
  • start low and go slow in older patients
  • review regularly
  • explain clearly
143
Q

what is deprescribing?

A
  • the supervised withdrawal of inappropriate medicines
  • used increasingly as a response to polypharmacy
  • if adding a new drug, is it possible to subtract an existing one?
144
Q

what are corticosteroids?

A
  • synthetic versions of hormones produced by the adrenal glands
  • glucocorticoids eg. prednisolone
  • they inhibit the immune system: used to treat autoimmune conditions (eg. lupus, or RA when the immune system attacks the body)
  • they suppress inflammation: reduce redness and swelling, useful in inflammatory conditions eg. asthma, eczema, temporal arteritis
145
Q

corticosteroid anti-inflammatory effects

A
  • inhibit vasodilation and increased vascular permeability — altered fluid retention at site of tissue damage
  • reduce number of circulating lymphocytes and inhibit emigration to damaged tissue
  • inhibit cytokine expression (eg. IL1 and TNF, both integral to cell mediated immune response)
  • inhibit production of phospholipase — prevents formation of arachidonic acid and inflammatory mediators
146
Q

what is important when stopping corticosteroid medication and why?

A

taper dose before stopping — to prevent withdrawal symptoms, to allow the adrenal glands to start secreting cortisol again, to prevent relapse of the underlying condition

147
Q

what must you consider when prescribing corticosteroids?

A
  1. bone protection eg. bisphosphate
  2. gastric protection eg. proton pump inhibitor
  3. monitor blood glucose

REVIEW REGULARLY

148
Q

in patients, the effects of glucocorticoid receptor agonists often show a time lag of what?

A

hours to days

149
Q

when glucocorticoid receptors act via a transactivation mechanism, they bind to a region of DNA known as what?

A

hormone response element

150
Q

what hormone regulates the resorption of calcium from bone?

A

parathyroid hormone

151
Q

what hormone regulates the absorption of calcium for bone calcification?

A

calciferol (1,25-hyroxy vitamin D3)

152
Q

what cell produces osteoprotegerin?

A

osteoblasts

153
Q

what does PTH cause?

A
  • increased phosphate and calcium absorption from the intestine and bone
  • increased phosphate excretion by the kidneys
  • causes kidneys to retain Ca ions
154
Q

where do gram positive bacteria survive best?

A

in dry and dusty conditions

155
Q

why are osteoclasts multinucleated?

A

to increase the lifespan of the cell

156
Q

where do osteoclasts originate from?

A

haemopoietic stem cells

157
Q

who she prednisone not be given to?

A

patients who have a history of hepatic failure

158
Q

why does spongy bone differ from compact bone?

A

because spongy bone is composed of trabeculae that are orientated along lines of stress

159
Q

describe the order of bone fracture

A
  1. formation of a hepatoma at the site of fracture
  2. migration of fibroblasts to the fracture site
  3. bridging of broken ends of bones by a fibrocartilaginous callus
  4. osteoblast production of trabeculae and bony callus formation
  5. resorption of remaining bone fragments and remodelling of bone
160
Q

medications, slower mobility, lack of proper fluid intake, and poor diet can contribute to what common symptoms in the elder population?

A

urinary incontinence

161
Q

osteoclasts derive from which stem cell progenitor? osteoblasts?

A

haematopoietic stem cells

osteoblasts = osteoprogenitor cells

162
Q

how to glucocorticoids contribute to osteoporosis?

A

by stimulating reabsopriton of Ca ions

163
Q

during which stage of healing is collagen remodelled?

A

maturation phase

164
Q

what constitutes severe established osteoporosis?

A

recorded fragility fracture

165
Q

where does a ‘dysgerminoma’ cancer originate?

A

germ cell of the ovaries

166
Q

what is a paraneoplastic syndrome?

A

tumour or host cells releasing hormones and cytokines that cause changes in the body and tissue destruction

167
Q

what are 3 causes of lordosis?

A

obesity, pregnancy, weakness in abdominal muscles

168
Q

what is the approximate average bone density?

A

1500 kg/m3

169
Q

osteoporosis

A

loss of entire bone substance

PBL SEM 1 (9 decks)

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