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Phase 3b > 12/03/2021 [back muscles, micturition, UTIs, CRMO, rheumatic fever]] > Flashcards

12/03/2021 [back muscles, micturition, UTIs, CRMO, rheumatic fever]] Flashcards

1
Q

Associated movements of the superficial, intermediate and deep muscles

A

Superficial - shoulder movements
Intermediate - thoracic cage movements
Deep - vertebral column movements

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2
Q

Where do all the superficial back muscles originate and attach onto?

A

originate - vertebral column

attach - bones of the shoulder [clavicle, scapula, humerus]

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3
Q

Muscles in the superficial back [from most superficial to deep]

A

Trapezius, latissimus dorsi, levator scapulae, rhomboids

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4
Q

Actions of the trapezius

A

The upper fibres of the trapezius elevates the scapula and rotates it during abduction of the arm. The middle fibres retract the scapula and the lower fibres pull the scapula inferiorly

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5
Q

What is the most common cause of accessory nerve damage?

A

The most common cause of accessory nerve damage is iatrogenic (i.e. due to a medical procedure). In particular, operations such as cervical lymph node biopsy or cannulation of the internal jugular vein can cause trauma to the nerve

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6
Q

How is accessory nerve damage tested for?

A

To test the accessory nerve, trapezius function can be assessed. This can be done by asking the patient to shrug his/her shoulders. Other clinical features of accessory nerve damage include muscle wasting, partial paralysis of the sternocleidomastoid, and an asymmetrical neckline

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7
Q

Actions of latissimus dorsi

A

Extends, adducts, medially rotates the upper limb

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8
Q

Action of the levator scapulae

A

Elevates the scapula

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9
Q

Action of the rhomboids

A

Rhomboid major - retracts and rotates the scapula

Rhomboid minor - retracts and rotates the scapula

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10
Q

What is in the intermediate group of muscles in the back?

A

Serratus posterior superior

Serratus posterior inferior

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11
Q

Actions of the intermediate muscles of the back

A

Serratus posterior superior - elevates ribs 2-5

Serratus posterior inferior - depresses ribs 9-12

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12
Q

Which group of muscles are known as the intrinsic muscles of the back and why?

A

The deep muscles develop embryologically in the back, and are thus described as intrinsic muscles. The superficial and intermediate muscles do not develop in the back, and are classified as extrinsic muscles.

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13
Q

Superficial deep muscles of the back

A

Spinotransversales

  • splenius capitis
  • splenius cervicis
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14
Q

Action of the spinotransversalis

A

Rotates head to the same side

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15
Q

Intermediate deep muscles of the back

A

Erector spinae

  • iliocostalis
  • longissimus
  • spinalis
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16
Q

Where do all the intermediate deep muscles attach?

A

Lumbar and lower thoracic vertebae
Sacrum
Posterior aspect of the iliac crest
Sacroiliac and supraspinous ligaments

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17
Q

Action of the intermediate deep muscles

A

Acts unilaterally to laterally flex the vertebral column. Acts bilaterally to extend the vertebral column and head

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18
Q

Major muscles in the deep deep back [there are other minor deep intrinsic muscles]

A

Semispinalis, multifidus and rotatores

[mainly stabilise vertebral column]

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19
Q

Area of the brain involved in the storage of urine

A

Pontine continence centre [L-region of the pons]

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20
Q

Signal sent from the brain to stimulate micturition

A

Pons -> sympathetic nuclei [spinal cord] -> detrusor muscle and IUS

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21
Q

How do impulses travel from the spinal cord to the bladder?

A

Via the hypogastric nerve [nerve roots T10-12]

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22
Q

What does the hypogastric nerve stimulate?

A

Relaxation of the detrusor muscle in the bladder wall – via stimulation of β3-adrenoreceptors in the fundus and the body of the bladder.
Contraction of the IUS – via stimulation of α1-adrenoreceptors at the bladder neck

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23
Q

What type of innervation is the storage phase?

A

Sympathetic

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24
Q

What type of control is the EUS under?

A

Voluntary somatic control

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25
Q

Where do impulses travel to the EUS from?

A

The pudendal nerve [S2-4] to nicototinic [cholinergic] receptors on the striated muscle, resulting in contraction of the sphincter

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26
Q

Type of innervation is the pudendal nerve?

A

Somatic voluntary control

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27
Q

What can spinal cord lesion above T12 cause?

A

reflex bladder

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28
Q

Explain a reflex bladder

A

In an upper motor neurone lesion, sympathetic input to the bladder is lost, leading to an inability for the detrusor muscle to relax, or the IUS to contract.

Afferent signals via the sensory pelvic nerve are also unable to reach the brain, and so the EUS remains constantly relaxed. The result is decreased bladder capacity and detrusor overactivity. The parasympathetic system initiates detrusor wall contraction in response to bladder wall stretch, resulting in the bladder automatically emptying as it fills. This is known as a reflex bladder.

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29
Q

Causes of a reflex bladder

A

Trauma and MS

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30
Q

What can lesion in the pontine continence centre [PCC] cause?

A

Lesions in the pons can lead to a complete loss of voiding control and the inability to store urine. In damage to the PCC, sympathetic input to the bladder is lost. This results in the same symptoms as a reflex bladder, although the damage is in a different location

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31
Q

Causes of PCC incontinence

A

Typical causes of such brain lesions are strokes, brain tumours and the degeneration of dopaminergic neurones in Parkinson’s disease

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32
Q

Pharmacological Tx of urinary incontinence secondary to neurological insults

A
  • Anticholinergics(e.g. Oxybutynin, Tolterodine) which reduce parasympathetic input to the bladder
  • β3-adrenoceptor agonists(e.g. Mirabegron) bind to β3-receptors on the detrusor muscle and stimulate relaxation of the muscle. Therefore, these drugs can be used to increase the bladders capacity to store urine in the treatment of urge urinary incontinence
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33
Q

SE of anticholinergics

A

More likely to result in anticholinergic side effects such as a dry mouth or constipation, so are used less frequently. Oxybutynin particularly should be avoided in elderly frail patients due to an increased falls risk

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34
Q

other types of Tx for urinary incontinence

A

Other possible therapies include the injection of botulin toxin A, sacral nerve stimulation, and surgical procedures such as Augmentation enterocystoplasty or urinary diversion.

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35
Q

What is the stress-relaxation phenomenon?

A

Most of the time, the bladder (detrusor muscle) is used to store urine. As it fills, the rugae distend and a constant pressure in the bladder (intra-vesicular pressure) is maintained.

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36
Q

urinary flow rate in the full bladder

A

20-25ml/s in men

25-30ml/s in women

37
Q

Bladder capacity

A

Whilst the capacity of the bladder varies from roughly 300-550ml, afferent nerves in the bladder wall signal the need to void the bladder at around 400ml of filling

38
Q

Go through neural control of micturition

A

image

39
Q

Type of regulation is passing urine under?

A

Parasympathetic control

40
Q

Go through parasympathetic stimulation of the pelvic nerve

A

There is subsequent parasympathetic stimulation to the Pelvic Nerve (S2-4) causing a release of ACh, which works on M3 muscarinic ACh receptors on the detrusor muscle, causing it to contract and increase intra-vesicular pressure. The pontine micturition centre also inhibits Onuf’s nucleus, with a resultant reduction in sympathetic stimulation to the internal urethral sphincter causing relaxation

41
Q

Conscious control of micturition

A

Finally, a conscious reduction in voluntary contraction of the external urethral sphincter from the cerebral cortex allows for distention of the urethra and the passing of urine.

42
Q

How voluntary passing of urine in males differs to females

A

In the female, urination is assisted by gravity, while in the male, bulbospongiosus contractions and squeezing along the length of the penis helps to expel all of the urine

43
Q

Causes of urinary retention

A

Urinary retention has a variety of causes:

Benign prostatic hyperplasia (BPH) – this is the most common cause
Nerve dysfunction
Infection
Constipation
Drugs – including anticholinergics, antidepressants and opioids

44
Q

How do patients typically present for urinary retention problems?

A

Patients typically present with intermittent flow, straining, vesical tenesmus (the feeling of incomplete emptying of the bladder following urination) and hesitancy (a delay between trying to urinate and the flow beginning).

45
Q

Cx of urinary retention

A

Complications include incontinence, nocturia (the need to urinate at night), pain, hypertension, high frequency, hydronephrosis (high vesical pressure can push urine back up ureters), kidney failure, sepsis. Retention leading to complete anuria (inability to pass urine) can cause the bladder to significantly stretch and possibly tear.

46
Q

Short-term and long-term Tx for urinary incontinence

A

In an acute setting treatment includes urinary catheterisation, a prostatic stent or a suprapubic cystostomy can be used. Long-term patients’ treatment is dependent on cause, with the most common cause, BPH, having pharmacological (alpha blocker, 5-alpha-reducatase inhibitor) and surgical (prostatectomy, transurethral resection of the prostate) treatment options

47
Q

What is a UTI known as if it effects the bladder?

A

Cystitis

48
Q

What is a UTI known as if it affects the kidneys?

A

Pyelonephritis

49
Q

Common Sx of a lower UTI

A

Pain with urination, frequent urination, feeling need to urinate despite empty bladder

50
Q

Sx kidney infection

A

fever and flank pain [usually in addition to Sx of a lower UTI]
rarely, the urine may be bloody

51
Q

Commonest cause of a UTI

A

E.coli [though sometimes other bacteria/fungi may be ther cause]]

52
Q

Uncomplicated UTI Tx

A

Short course Abx; e.g. nitrofurantoin, trimethoprim/sulfamethoxazole

53
Q

Complicated UTI Tx

A

Longer course IV Abx

54
Q

In those that have bacterai /WBC in their urine but no Sx [of a UTI], what Tx recommended?

A

Not Abx [pregnancy an exception]

55
Q

How common are UTIs?

A

Up to 10% of women have a UTI in a given year.

Occur most frequentl ages 16-35.

56
Q

How long do UTIs commonly last in younger women?

A

6d

57
Q

Common Sx of UTi in children?

A

May be a fever only.

Infants may feed poorly, vomit, sleep more, show signs of jaundice.

58
Q

Sx of UTI elderly

A

Vague with incontinence, change mental status [delirium], fatigue only Sx.
Some can present with infection of blood [sepsis] as only Sx.

59
Q

Cause of UTIs micrboially

A
  • E.coli from the gut in 80-85% community acquired UTIs, with staphylococcus saprophyticus being 5-10%.
    Rarely due to viral/fungal infections.
  • Healthcare-associated UTIs broader range: E.coli [27%], Klebsiella [11%], Pseudomonas [11%], candida albicans [9%], enterococcus [7%] amongst others.
60
Q

In young women what is the common cause?

A

Sexual activity 75-90% bladder infections.

61
Q

Why are older women more at risk of UTIs?

A

Women are more prone to UTIs than men because, in females, the urethra is much shorter and closer to the anus.[32] As a woman’s estrogen levels decrease with menopause, her risk of urinary tract infections increases due to the loss of protective vaginal flora.[32] Additionally, vaginal atrophy that can sometimes occur after menopause is associated with recurrent urinary tract infections

62
Q

Prevention of UTIs

A

A number of measures have not been confirmed to affect UTI frequency including: urinating immediately after intercourse, the type of underwear used, personal hygiene methods used after urinating or defecating, or whether a person typically bathes or showers.[4] There is similarly a lack of evidence surrounding the effect of holding one’s urine, tampon use, and douching.[32] In those with frequent urinary tract infections who use spermicide or a diaphragm as a method of contraception, they are advised to use alternative methods.[7] In those with benign prostatic hyperplasia urinating in a sitting position appears to improve bladder emptying which might decrease urinary tract infections in this group.[51]

Using urinary catheters as little and as short of time as possible and appropriate care of the catheter when used prevents catheter-associated urinary tract infections.[35] They should be inserted using sterile technique in hospital however non-sterile technique may be appropriate in those who self catheterize.[37] The urinary catheter set up should also be kept sealed.[37] Evidence does not support a significant decrease in risk when silver-alloy catheters are used

63
Q

What is CRMO?

A

Chronic recurrent multifocal osteomyleitis [CRMO]

64
Q

What is CRMO?

A

Chronic recurrent multifocal osteomyleitis [CRMO]or chronic nonbacterial osteomyelitis (CNO), is a disorder that causes bone pain due to inflammation in the bones not caused by infection

65
Q

Average age of Dx for CRMO

A

The average age that CRMO starts is 9 to 10 years. More girls are affected than boys

66
Q

Cause of CRMO

A

CRMO is an auto-inflammatory disorder, meaning the immune system attacks the bones causing inflammation, even though there is no infection. A small fraction of people with CRMO have a genetic component. Some families have more than one person with CRMO

67
Q

Common Sx of CRMO

A

Bone pain is the most common symptom. There is usually tenderness at the affected site (it hurts to be pushed on). The pain can cause the person to avoid using the affected body part. Some people with CRMO can develop arthritis (joint swelling). Fatigue is common during active disease.

68
Q

Dx of CRMO

A

Diagnosis is based on exam, imaging (such as x-rays, bone scan or MRI), bone biopsy, and laboratory (blood) tests. Lab tests are normal in most people, but can show anemia (blood doesn’t carry enough oxygen through your body) and elevated markers of inflammation (ESR, CRP) in others. Bone that has been altered or damaged can be seen on x-ray, bone scan and MRI. MRI is the most sensitive type of imaging to find signs of CRMO. Bone biopsy may be needed to rule out infection or cancer. The biopsy in CRMO usually shows acute (short-term) or chronic (long-term) inflammation

69
Q

Tx of CRMO

A

Treatment of CRMO depends on how severe it is and which bones it affects. Some people respond to non-steroidal anti-inflammatory medications (NSAIDs), such as naproxen, meloxicam or indomethacin. These medications can cause stomach upset and easy bruising. People on these medications long-term should have lab monitoring for liver and kidney function.

People with continued pain and active bone lesions can require stronger immunosuppressive medications, such as methotrexate. Methotrexate can cause nausea and requires regular lab monitoring. It can be dangerous in people who drink alcohol and can cause birth defects if taken during pregnancy.

Additional treatment options include biologic medications, such as etanercept, adalimumab or anakinra, which are injectable medications, or infliximab, which is an IV infusion. Methotrexate and biologic medications are immunosuppressive. People taking these medicines are at an increased risk of infection and should be evaluated by a doctor if they develop fever or symptoms of infection. People must be screened for tuberculosis (TB) prior to starting biologic medications.

Bisphosphonates such as pamidronate and zoledronic acid are another type of treatment for CRMO. These medicines are IV infusions used to treat bone conditions such as osteoporosis. Bisphosphonates can cause flu-like symptoms for a few days after the infusion

70
Q

When does rheumatic fever occur?

A

After streptoccal pharyngitis [throat inflammation] from streptococcus pyogenes [strep throat]

71
Q

Which protein does immune system cross react with in rheumatic fever?

A

M protein from streptococcus pyogenes [molecular mimicry] to heart/joints/skin brain

72
Q

Type of reaction is molecular mimicry?

A

Type 2 hypersensitivty

73
Q

How common do people who get strep throat get rheuamtic fever

A

About 3% in LEDCs

74
Q

Acute RF Sx

A
  1. Migratory polyarthritis
  2. Pancarditis [endocarditis, myocarditis, pericarditis]
  3. Subcutaneous nodules [collagen lumps]
  4. Erythema marginatum [rings]
  5. Sydenham chorea
75
Q

Commonly affected valve in pancarditis

A

Mitral valve [though aortic valve can also be affected]

76
Q

Myocarditis histology

A

Aschoff body: areas of fibrinoid necrosis

77
Q

What is the most common cause of death in RF?

A

Myocarditis -

78
Q

Sx of pericarditis

A

Pain, friction rub [which can be heard stethscope]

79
Q

What is syndenham chorea?

A

Rapid movements face+arms = due to basal ganglia

damage later in disease

80
Q

Jones criterai

A

5 acute Sx + previous strep infection [2-3 weeks after] = diagnosis

81
Q

Minor criterai for RF

A

Fever, joint pain
Increased WCC, APP, fibriogen, ESR
Changes in ECG

82
Q

Tx for RF

A

Usually resolves with rest
+ anti-inflammatory medication
+ antibiotics

83
Q

Subset Sx in RF

A

Poststrep reactive arthritis -> joint Sx

PANDAS -> neuropsychiatric Sx

84
Q

Which can acute RF lead to?

A

Chronic rheumatic heart disease

85
Q

Chronic rheumatic heart disease PP

A

Valves [typically mitral valve] become fibrous -> stenosis/regurgitation. Risk of IE.

86
Q

How to prevent acute-> chronic RF?

A

Reduce strep infections = prolonged antibiotics [can be a lifetime of Abx]

87
Q

Acronym for kawasaki disease

A 
C - conjuctivitis
R - rash
A - adenopathy
S - strawberry tongue
H - hand
and burn [over 5d of fever]
88
Q

Dangerous Cx of kawasaki

A

Coronary artery aneurysms

Phase 3b (10 decks)

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