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Specialties including Infectious Disease Flashcards

1
Q

suggest 5 classes of drug which are responsible for blocking cell wall synthesis

A
  1. penicillins
  2. cephalosporins
  3. monobactams
  4. carbapenems
  5. vancomycin
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2
Q

what is the method of action of quinolone drugs?

A

they will act to inhibit DNA synthesis

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3
Q

metronidazole will act by breaking bacterial DNA - true or false?

A

true

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4
Q

sulphonamides will act by blocking cell wall synthesis - true or false?

A

false

sulphonamides act by inhibiting folic acid.

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5
Q

suggest 4 drugs responsible for inhibition of protein synthesis

A
  1. aminoglycosides
  2. tetracyclines
  3. macrolides
  4. fusidic acid
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6
Q

An elderly man has been admitted to hospital with acute onset disorientation, visual hallucinations and agitation. He has no psychiatric history and lives alone and requires no support. What is the most likely diagnosis

A

Delirium

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7
Q

A man is admitted to A&E after being found semi-conscious in the street. He is unkempt. And does not have any information on his person; he appears to be street homeless. In A&E he has a tonic clonic seizure which is self-limiting after 3 minutes. The man is postictal for a short time but soon becomes restless, tremulous and sweaty. His speech is rambling, and he complains about the bed sheets being filthy and ‘filled with mites’. He is tachycardic with a blood pressure of 186/114 mmHg.

  1. What is the most likely diagnosis?
  2. You order a full set of bloods on this man. Which of the following results would be most indicative of the underlying cause of his delirium
A
  1. Delirium tremens

2. low serum vitamin b12

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8
Q

A 73 y/o woman is admitted to hospital with an infective exacerbation of chronic obstructive pulmonary disease (COPD). Apart from COPD and hypertension she has no other medical problems. On the 3rd day of her admission, she becomes acutely confused. During the night she is awake, shouting constantly for her husband, claiming that the nurses are prison guards and that they are keeping her against her will. She is slightly calmer the day after. You are the FY1 on call and are asked to come and see her over the weekend as the nurses are worried it will happen again at night. What should your initial management be

A

prescribe nothing at this stage

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9
Q

what is the vaccine for HIV?

A

there isnt one

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10
Q

what is an anthroponoses?

A

a disease causing agent is carried by humans and then is transferred to other animals

includes influenza (birds and pigs), strep throat (dogs), leishmaniasis (dogs)

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11
Q

how would you treat an aspergillus species infection?

A

amphotericin B, isavuconazole, itraconazole.

fluconazole has no effect

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12
Q

43 y/o female visits GP complaining of 4 week history of fever, fatigue, low mood and lower back pain. she had visited China in the previous month and mentioned she was drinking plenty of goats milk as this was the only type of milk available. what is the most likely infective cause?

A

Brucellosis

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13
Q

what is the treatment for cellulitis?

A

flucloxacillin and benzylpenicillin

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14
Q

treatment of C. Dificile overgrowth?

A

fidaxomicin
vancomycin
metronidazole

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15
Q

what is the treatment for cryptococcus sp?

A

amphotericin B, flucytosine and fluconazole

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16
Q

what is the most common likely cause of an outbreak of nausea and vomiting on a cruise ship?

A

norovirus

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17
Q

what is the commonest cause of traveller’s diarrhoea?

A

enterotoxigenic escherichia coli

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18
Q

what is the commonest bacterial cause of infective diarrhoea in the UK

A

campylobacter

a suitable oral rehydration therapy - ORT - solution would be sodium chloride and glucose

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19
Q

a 3 year old boy presents with his m,other to his GP with a 2 day history of fevers, vomiting and diarrhoea. his mother mentions that several other children at nursery have been off sick this week with the same problem. what is the most likely cause?

A

rotavirus

the most appropriate management for gastroenteritis is oral rehydration, advice and discharge home

investigations would include a stool sample for microscopy, culture and sensitivities

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20
Q

staphylococcus aureus is likely to cause blood-stained diarrhea - true or false?

A

false.

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21
Q

how is the best possible way to diagnose influenza virus?

A

viral culture

influenza vaccines depend upon up to date knowledge of circulating strains

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22
Q

what are the most important tests for suspected plasmodium falciparum infection?

A

a malaria film and antigen test

treat with IV quinine if extremely unwell otherwise if well give oral preparations

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23
Q

27 yo returning from a holiday in africa presents to ED with one week history of fever, sweats, HA, malaise and lethargy. O/E her temperature is 39 and CV and GI examinations are unremarkable. what is the most likely diagnosis?

A

malaria.

diagnose with a thick and thin blood film

treat with quinine

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24
Q

what is the triad of neuroborreliosis?

A
  1. facial nerve palsy
  2. radicular pain
  3. lymphocytic meningitis
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25
Q

what is a zoonoses?

A

a zoonoses is an infectious disease of animals that can naturally be transmitted to humans. some diseases are transmitted from animals but are not zoonoses as they depend on the human host for part of their life-cycle

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26
Q

what is the prognostic system that determines overall mortality risk for sepsis?

A

SOFA score >2

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27
Q

what component of neisseria meningitidis causes septic shock?

A

lipopolysaccharides

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28
Q

what is the management of a woman with sepsis

A
  1. prompt IV antibiotics administration
  2. antipyretic measures
  3. IV fluids
  4. referral to hospital
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29
Q

suggest 6 criteria in systemic inflammatory response syndrome (SIRS)

A
  1. T <36 or >38
  2. HR >90
  3. RR> 22
  4. PaCO2 <32
    WBC >12000 or < 4000
    > 10% bands
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30
Q

what is sepsis?

be specific

A

life-threatening organ dysfunction caused by dysregulated host response to infection.

SIRS + Infection. organ dysfunction can be identified as an acute change in total SOFA score >2 points consequent to the infection

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31
Q

what is severe sepsis?

A

Sepsis + end organ damage or insufficient flow

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32
Q

what is septic shock?

A

clinical construction of sepsis with persisting hypotension requiring vasopressors to maintain MAP >65 mmHg and having a serum lactate of >2 mmol/L despite adequate fluid resuscitation
- severe sepsis and hypotension even with IV fluids

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33
Q

what are the risk factors for developing sepsis?

A
  1. age
  2. comorbidities
    a. COPD
    b. diabetes
    c. congestive cardiac failure
    d. chronic renal failure
    e. disseminated malignancy
  3. immunosupression
  4. previous surgery / hospitalisation
  5. occupation
  6. travel
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34
Q

what is the typical presentation of a patient with sepsis?

A
  1. fever>38
  2. hypothermia in elderly young and immunosuppressed
  3. tachycardia
  4. tachypnoea
  5. altered consciousness
  6. hyperglycaemia (in absence of diabetes)
  7. confusion
  8. psychosis
  9. jaundice
  10. increased liver enzymes
  11. decreased albumin
  12. increased PT
  13. decreased platelets
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35
Q

what is pathogenesis of sepsis?

A
  1. Gram +
    a. Lipoteichoic acid (LTA)
  2. Gram -
    a. microbial associated molecular pattern
    i. LPS - lipopolysaccharide
    ii. . muramyl dipeptides
    b. superantigens
    i. staphylococcal toxic shock syndrome (TSST)
    ii. streptococcal exotoxins
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36
Q

what investigations would you like to carry out for a patient with suspected sepsis?

A
  1. quick sepsis-related organ failure assessment (q-SOFA)
    - hypotension
    - altered mental state
    - tachypnoea
  2. risk stratification tool
  3. sepsis 6
    a. take blood cultures (make diagnosis, if there is a spike in temperature then take 2 sets)
    b. take blood lactate (type A is a marker of tissue hypoperfusion; type B is a marker of mitochondrial toxins, alcohol, malignancy)
    c. take urine output (if low a marker of renal dysfunction)
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37
Q

what is the management of sepsis?

A 
1. oxygen (aim 94-96%)
2, fluid challenge 
3. IV antibiotics 
   a. amoxicillin 
   b. gentamicin 
   c. metronidazole 
   d. vancomycin

HDU referral

  • indications
    1. low BP responsive to fluids
    2. lactate >2 despite fluid resuscitation
    3. elevated creatinine
    4. oliguria
    5. liver dysfunction
    6. bilateral infiltrates
    7. hypoxaemia

ITU
- requires sedation,, intubation and ventilation
indicated in septic shock and multi-organ failure

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38
Q

when is anaesthesia used?

A
  1. perioperative medicine, intraoperative care, post operative care
  2. pain: chronic and acute
  3. intensive care/critical care
  4. hyperbaric medicine (delivers 100% oxygen tat higher atmospheric pressure)
  5. pre hospital care/retrieval/transfer
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39
Q

`what are the different types of anaesthesia?

A
  1. general
  2. regional
  3. local
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40
Q

what are the pros and cons of using balanced anaesthesia using the anaesthetic triad?

A

PROS

allows flexibility of control

  1. awake (Y/N)
  2. analgesia (none/opiate/loca)
  3. muscle relaxation (Y/N)
  4. airway management (none, mask, LMA (laryngeal mask airway) or EET)

tailored technique to patient, operation and duration

CONS

polypharmacy - increased risk of negative drug interactions
muscle relaxation requires airway control and artificial ventilation
separation of relaxation and hypnosis means the patient may become aware during the procedure

all anaesthetics have physiological changes on the body - even loca and general anaesthetic!!

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41
Q

what are the main drugs that are used via IV drug infusion?

A

propofol and thiopentone

PROS - they will have a rapid onset due to arm-brain circulation and take roughly 20 seconds

CONS - it is easier to overdose and there is generally a rapid loss f airway control and apnoea is very common so breathing aids are required.

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42
Q

what are the main drugs that are used as inhaled general anaesthetics?

A

sevoflurane (halothane hydrocarbon). it is indicated in young children and patients who have airway compromise. it is slow working (CONS)

43
Q

what is the role of anaesthetist pre-operatively?

A
  1. assess the patient
    a. history for the known comorbidities (including severity and control), systemic enquiry (to assess unknown comorbidities), exercise tolerance, cardiorespiratory disease/previous surgery and anaesthesia, drugs and allergies
    b. examinations and investigations
  2. identify high risks
  3. optimise
  4. minimise risks
  5. inform and support patient decisions
  6. consent
44
Q

what things must an anaesthetist take into account before surgery?

A
  1. normal physiological stress response - CVS, renal, respiratory and metabolic
  2. blood loss
  3. fluid shifts
  4. drug interactions
  5. known comorbidities and unknown pathologies
  6. nature of surgery
  7. post op care
45
Q

what is the ASA grading scale?

A

it is used to identify the risks of operating on a patient

ASA 1-5
1 - otherwise healthy patient
2 - mild to moderate systemic disturbance
3. severe systemic disturbance
4. life-threatening disease
5 - moribund patient; will not survive for 24h with or without surgery

46
Q

aside from ASA grading scale what other risk assessment questionnaires are available for anaesthetists?

A
  1. ASA grading scale
  2. Lee’s revised cardiac risk index
  • risk stratification; give 1 point for each positive risk factor
    a. high risk surgery
    b. ischaemic heart disease
    c. congestive cardiac failure
    d. cerebrovascular disease
    e. diabetes mellitus
    f. serum creatinine > 180

greater than 3 points will indicate there is a high risk of a cardiac event

47
Q

in particular reference to neurotransmitters, what is GABA?

A

GABA is a neurotransmitter whose function is to:
- reduce the activity of neurons to which it binds.

this means it will most likely reduce fear/.anxiety when neurons become over-excited. this, it is hypothesized that gabapentin inhibits transmitter release and attenuates post-synaptic excitability (hence diminishing seizure activity)

48
Q

how do you monitor the levels of consciousness in anaesthetics?

A
  1. loss of verbal contact
  2. movement
  3. respiratory problems
  4. EEG changes
  5. stages or planes of anaesthesia
49
Q

what are some typical airway complications using general anaesthetic?

A
  1. obstruction
  2. laryngospasm - forced reflux adduction of the vocal cords due to light plane of anaesthesia. it can result in complete airway obstruction and is often unresolved by simple maneuvers.
  3. aspiration - gastric contents, blood and surgical debris
50
Q

suggest 5 general monitoring requirements in general anaesthetic

A
  1. SpO2 and ECG
  2. respiratory rate and blood gases
  3. agent monitoring
  4. temperature
  5. urine output
51
Q

what is the main ion channel blocked in local anaesthetics (LA)?

A

sodium channel blockade which prevents the propagation of action potentials. they act indiscriminately on any number of tissues as all excitable membranes in tissue contain sodium channels. LA drugs must be unionised to cross axon membranes, thus are less efficient in damaged tissue (relatively lower pH)

52
Q

describe the neuro-pharmaceutical basis behind the treatment of myasthenia gravis

A
  1. Non-depolarizing NMJ Blockers are competitive blockers of Nicotinic Ach receptors at the NMJ, thus their use is reversible once there is enough [Ach] to overcome the competitive blockers. In emergency situations of reversal (e.g. Muscle relaxant overdose) and increase of anticholinesterases will stop the removal of Ach, thus increasing [Ach] and causing reversal of respiratory distress. These drugs are essentially medical exploitations of what happens in Myasthenia Gravis.

suxamethonium

53
Q

give 2 examples of non-opioid analgesics

A

aspirin and paracetamol

The most effective form of treatment is through using multi-modal analgesia, which will help block the pain pathway at various sites

54
Q

give an example of weak opioids

A

tramadol, codeine

The most effective form of treatment is through using multi-modal analgesia, which will help block the pain pathway at various sites

55
Q

give an example of a strong opioid

A

morphine and fentanyl and methadone and oxycodone

The most effective form of treatment is through using multi-modal analgesia, which will help block the pain pathway at various sites

56
Q

what is the WHO pain ladder?

this is only applicable to nociceptive pain

A
  1. mild to moderate pain
    - non-opioids (aspirin), NSAID (ibuprofen, naproxen and diclofenac) or paracetamol
  2. moderate to severe pain
    - mild opioids (codeine) with or without non-opioids
  3. severe pain
    - strong opioids (morphine) with or without non-opioids

this is only applicable to nociceptive pain

57
Q

name 7 different routes of delivery of analgesia

A
  1. oral
  2. rectal
  3. subcutaneous
  4. transdermal
  5. intramuscular
  6. intravenous
  7. epidural
  8. spinal
58
Q

what do COX1 and COX2 inhibitors do?

A

they inhibit COX1 and 2 acting arachidonic acid to convert various prostaglandins and thromboxanes which are pro-inflammatory. this will thus block pain at nerve endings

59
Q

what are some of the adverse effects of using opioids?

A
  1. respiratory depression -
    a. hypoxaemia
    b. respiratory acidosis (block specialised respiratory neurons in the brainstem)
  2. vasodilation
  3. bradycardia
  4. myocardial depression
  5. CNS sedation euphoria
  6. miosis
  7. urinary retention
  8. constipation (decreased peristalsis therefore should be given with laxatives)
  9. sphincter of oddi spasm (hepatopancreatic sphincter)
  10. nausea and vomiting
60
Q

what are some signs of opioid toxicity?

A
  1. agitation
  2. confusion
  3. myoclonic jerks
  4. hallucinations (especially in peripheral vision)

if you suspect opioid toxicity then rehydrate and lower dose but do not stop completely

61
Q

what should you do if you suspect opioid toxicity?

A

if you suspect opioid toxicity then rehydrate and lower dose but do not stop completely

62
Q

what is meant by opioid tolerance?

A

the long use of strong opioids can lead to tolerance (body becomes less susceptible to opioid use, thus, requires higher doses to maintain pain control) and dependence (due to stimulation of the reward pathways in the brain).

thus opioids must be weened off slowly, otherwise one runs the risk of withdrawal syndrome, with symptoms including 
a. strong cravings
b. nausea and vomiting 
c. cramps
d sweating 
e. muscle aches 
f. shakes 
g. insomnia 
h. agitation

opioids are renally excreted and toxicity may occur if there is impaired renal function

63
Q

what is the most common ADR with paracetamol (acetaminophen)

A

overdose leading to liver damage. it is the most common cause for acute liver failure in the UK

Chronic alcoholism decreases plasma levels of glutathione, thus, careful prescription of paracetamol should be used in alcoholics.

64
Q

what are gabapentin and pregamblin used to treat?

A

focal seizures with/without secondary generalisation and the treatment of (chronic) neuropathic pain

65
Q

what si pain?

A

pain is an unpleasant sensory and/or emotional experience associated with actual or potential tissue damage or described in terms of such damage.

66
Q

suggest 6 differences between acute and chronic pain

A
  1. acute pain is nociceptive but chronic pain is neuropathic
  2. acute pain derived directly from the pain receptors and chronic pain is pain that has lasted under 3 months
  3. acute pain is at areas of damaged tissues whereas chronic pain haas often no identifiable cause and damaged tissue may not be seen
  4. acute pain is well localised but chronic pain will persist after normal healing - not well localised
  5. acute pain will have a purpose (protecting against a noxious stimuli) but chronic pain has no protective function

6 acute pain is sharp or dull whereas chronic pain is burning or shooting

67
Q

what is neuropathic pain?

A

occurs due to an abnormal processing of pain signals due to nervous system damage or dysfunction. it needs to be treated differently from nociceptive pain.

there is an increased sensitisation of pain receptors (especially centrally) as well as an increase in neurons. There are also chemical changes to the dorsal horn leading to a loss of normal inhibitory modulation.

68
Q

how is pain transmitted to the brain?

A

there are many different nerve fibres that can be stimulated which will send impulses to the brain. within the dorsal horn of the spinal cord there are fibres that travel up the spinothalamic tract and transmit somatosensory signals to the brain

69
Q

what are some of the pros of using spinal and epidural anaesthesia?

A

pro - has limited respiratory effects which is good for patients with severe respiratory deficiencies and it also inhibits airway intubation. it is a good alternative to GA.

70
Q

what are some cons of using spinal and epidural anaesthesia?

A
  1. causes a fixed cardiac output which may be a problem if the patients are experiencing physiological vasodilation
  2. may cause infection
  3. may cause a hypocoagulable state, leading to hemorrhagic diathesis
71
Q

where is spinal anaesthesia injected?

A

it is injected into the subarachnoid space - between the arachnoid and the pia mater

it is indicated when analgesia is required below the level of T4 but motor and respiratory centres must remain intact. hypotension is a common side effect. it has a rapid onset

72
Q

where is epidural anaesthesia injected?

A

it is injected into the epidural space and is indicated in blocks at T4 and below.

there may be a segmental block affecting the areas to which the anaesthetic is injected. there is a slower onset but there is an extendable duration. hypotension may occur but is not as in common as spinal blocks. there is a distal sparing of sensation

73
Q

what are the 5 most common problems in the elderly?

A

the 5 I’s.

  1. imobility
  2. instability (falls)
  3. intellectual impairment
  4. incontinence
  5. iatrogenic
74
Q

what are the consequences of an ageing population?

A
  1. more people have comorbidities and there is an increased frailty (reduced ability to withstand illness without loss of function
  2. complexity of cases are increasing
75
Q

what is the definition of frailty?

A

impaired organ funciton and dyhomeostasis

76
Q

why are people getting oldeR?

A
  1. increased resources are available
  2. better economic conditions
  3. improved screening programmed with early diagnosis and treatment
  4. better outcome following major events - cardiac stroke and surgery
77
Q

what is comprehensive geriatric assessment?

A

a process to assess and manage illness in patients with frailty in which the doctor:

  1. determines what the problems are (multiple medical problems with multiple health domains)
  2. determines what we can reverse and what we can make better
  3. produce a management plan

the plan is goal centred and not problem centred ensuring we act in the patients best interest to deal with co-morbidities.

most diseases become more common with age, yet the least research is done on elderly care. there is very little evidence of drug efficacy for those who are 80+.

78
Q

what is cognitive impairment?

A
  1. an inability to remember things (memory loss)
  2. loss of executive function - an inability to plan things, an inability to react and interact with changes in the environment
  3. may include delirium and dementia or other dementia symptoms
79
Q

how do you measure cognitive impairment?

A
  1. memory loss - abbreviated mental test (AMT)

2. executive function - clock drawing, functional assessment (this is the test that the patient cares most about)

80
Q

what questions would you like to ask in a history when assessing the cognitive impairment of an individual?

A
  1. onset (when? sudden?)
  2. course (fluctuating or progressive)
  3. other associated features
  4. functional loss
81
Q

what are the 10 questions asked in the abbreviated mental test?

A
  1. how old are you?
  2. what time is it?
  3. what is the date?
  4. remember this address and repeat it after question 10
  5. can you identify 2 people in this room
  6. where are you from?
  7. who is the current monarch?
  8. when did WW1 end?
  9. what is your date of birth
  10. can you count backwards from 20?
  11. can you repeat the name of the address
82
Q

what is confusion?

A

confusion is a symptom characterised by speech or behaviour that is inappropriate to the given situation

83
Q

what are the causes of confusion?

A
  1. deafness
  2. receptive dysphasia - difficulty in comprehension of what other people are saying
  3. cognitive impairment leading to alterations in memory, learning, attention, language and problem solving and reasoning and perception (often secondary to stroke, haemorrhage, dementia and parkinson’s)
  4. expressive dysphasia - difficulty in expressing language
  5. dysphonia - an inability to produce sounds due to damage/loss of function at the vocal cords/
  6. dysarthria - an inability to create sounds due to neuronal damage of motor areas associated with speech production
  7. cultural dysharmony
84
Q

how do you diagnose confusion?

A
  1. clear medical history
    a. onset - when? how
    rapid?
    b. course - fluctuating or a progressive decline?
    c. any associated factors? - other illness like parkinson’s or any functional loss
85
Q

what is delirium?

A

dysfunction of the brain caused by a medical problem generally out with the brain. it is the commonest complication of hospital care in geriatrics

86
Q

what are the clinical features of delirium?

A
  1. altered LOC - hyperactive, hypoactive or mixed
  2. cognitive deficit or perceptual disturbances - esp a recent change
  3. acute onset and fluctuating course
  4. evidence of cause
  5. emotional lability
  6. altered sleep/wake cycles
  7. delusions
87
Q

what are the risk factors for delirium?

A
  1. when any susceptible brain interacts with harmful environmental factors such as infection
  2. predisposing factors - old age, frailty, dementia, PMH delirium, visual and hearing impairments, malnutrition, polypharmacy, co-morbidities (renal and hepatic are most common)
  3. precipitating risk factors - infection (not always UTI), dehydration, constipation, pain and immobility, medication use/withdrawal, sleep deprivation, hypoxia, alcohol/drug withdrawal or use, brain injury (stroke, tumour, bleed etc)
    - there are usually multiple predisposing factors at play at any given time
88
Q

briefly describe the pathology of delirium

A

delirium i spoorly understood however there is a correlation between:

a. overactive hypothalamic-pituitary-adrenal axis leading to overactive cortisol release
b. inflammation (causing high levels of inflammatory cytokines)
c. difference in neurotransmitter concentrations - decreased ACh and increased dopa

89
Q

what is the treatment of delirium?

A
  1. treat the underlying cause using both pharmacological and non-pharmacological treatments
    a. non-pharmacological = OT and encouragement of self-mobility, reorientation and reassurance, normalise sleep cycle, avoidance of catheterisation/physical restraints
    b. pharma = sedation/antipsychotics to allow for essential investigations, prevent patient endangerment or to relive distress or agitation only

= small doses of dopamine antagonists unless caused by alcohol withdrawal or Parkinsonism
= review all current pharma use and eliminate any possible culprits of delirium especially anticholinergics and sedatives.

90
Q

diagnostic investigations for delirium

A
  1. Full history and examination including PR
  2. FBC, UE, LFT, CA2+, CRP, TFTR, Glucose
    ECG
    CXR
91
Q

what are the complications of delirium

A
  1. increased risk of death
  2. increased length of hospital stay
  3. increased rates of institutionalisation following hospital stay
  4. persistent functional decline
92
Q

what are the main risk factors for dementia?

A

delirium

93
Q

how do you diagnose dementia?

A

mini mental state examination - may be falsely reassuring and intellectuallyu specific

94
Q

how do you treat dementia?

A
  1. non-pharma
    - cognitive stimulation
    - exercise
    - home care and support
  2. cholinesterase inhibitors
    - esp associated with alzheimer’s. not a cure but do help. RIVASTIGMINE AND GALANTAMINE
  3. antipsychotics - start low and go slow
  4. SSRIs
  5. mood stabilisers
95
Q

what is the differential diagnosis of dementia?

A
  1. structural brain lesion - frontal meningioma
  2. normal pressure hydrocephalus - incontinence, gait disturbance and cognitive impairment
  3. B12 deficiency
  4. chronic inflammatory disease so check ESR
  5. depression - apathy, poor concentration and functional decline
  6. hypothyroidism
  7. intracerebral bleeds and tumours
  8. hypercalcaemia
96
Q

what are the 3 main types of dementia?

A

vascular dementia
alzheimer’s
lewy body dementia

all three kinds will respond to cholinesterase inhibitors as most BPSD (behavioural and psychological symptoms of dementia) occur due to a lack of cholinergic activity

97
Q

what is alzheimer’s?

A

dementia of slow insidious onset that is characterised by a loss of recent memories followed by a progressive functional loss. there is also a change in personality and loss of inhibition and executive function etc. it is caused by complex changes in the brain. specifically there is development of beta amyloid plaques and neurofibrillary tangles leading to neuronal death and this brain shrinkage. risk factors include age and genetics.

98
Q

what is vascular dementia?

A

a gradual and permanent loss of brain fucntion caused by multiple mini strokes in the brain leading to multiple mini infarcts (holes in the brain). it is associated with widespread problems including gait issues, loss of executive function and patients often have known vascular factors.

99
Q

lewy body dementia it the most common cause of dementia in the elderly. describe its characteristics

A

it is characterised by a fluctuating decline of cognitive function etc caused by abnormal protein aggregates in cortical neurons. 2/3 patients will have movement dysfunctions so falls are common. severely underdiagnosed.

100
Q

what are the risk factors for falls?

A
  1. muscle weakness
  2. history of falls
  3. gait/balance/visual deficits
  4. use of assistive mobility aids
  5. arthritis
  6. depression
  7. cognitive impairment and dementia
  8. 80+ years old
101
Q

what is the aetiology of falls?

A

poor postural stability caused by decreased cerebral perfusion from cardiac output and vasomotor tone.

o Poor vision (cataracts, retinopathy, optic nerve/visual pathways abnormalities, refractory errors, retinopathy, stroke, hemianopia)
o Slips/trips due to environmental factors
o Gait/balance disorders; requires co-operation between sensory input (visual, vestibular, proprioceptive), central processing (cerebrum, cerebellum, basal ganglia and brain stem) and muscular activity e.g. Parkinson’s Disease
o Dizziness e.g. Vertigo (labyrinthitis, BPPV, Menieres Disease)
o Muscle weakness
o Polypharmacy
o Acute Illness - delirium, sepsis, dehydration
o Co-morbidities - CVD, PD, dementia
o Psychological esp. ‘fear of falling’

102
Q

what are 5 outcomes after a fall?

A
  1. soft tissue injury
  2. fracture (hip fractures are the most common)
  3. death
  4. subdural haematoma - chronic and common
  5. increased dependency and decreased QoL
  6. institutionalism
  7. terminal decline
103
Q

how are falls prevented?

A
  1. exercise
  2. health education classes
  3. better lighting
  4. clear hallways, stairs - reduce environmental causes of falls
  5. stop smoking
  6. reduce alcohol intake

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