7) repro, resp, psych Flashcards

1
Q

ACUTE BACTERIAL PROSTATITIS

  • age most commonly affected?
  • most common causative pathogen? 1
  • other causative organisms to consider? 2 (who in?)
  • risk factors? 4
A

men 20-50years

E. Coli = most common

consider chlamydia or gonorrhoea in men < 35

RISK FACTORS

  • recent urinary tract infection
  • urogenital instrumentation
  • intermittent bladder catheterisation
  • recent prostate biopsy
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2
Q

ACUTE BACTERIAL PROSTATITIS

  • where is the pain?
  • other local symptoms? 3
  • systemic symptoms? 3
  • examination to do? what find?
  • bedside tests to do? 2
A

SEVERE PAIN

  • lower back
  • perineum
  • pelvic
  • with defecation
  • acute dysuria
  • frequency
  • urgency
  • malaise
  • fevers
  • rigors

DRE (gently to avoid causing sepsis)
= tender + boggy prostate

  • urine dip
  • MSU
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3
Q

ACUTE BACTERIAL PROSTATITS

  • abx management? for how long?
  • possible complications? 3
A

PO fluroquinolone (eg ciprofloxacin) for 14 DAYS

complications

  • acute urinary retention
  • sepsis
  • prostatic abscess (needs drainage!)

nb if acute urinary retention and persistent fever: suprapubic catheterisation

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4
Q

aside from acute bacterial prostatits, what other types of prostatitis can you get? 2

breifly describe how they present + mx

A

CHRONIC BACTERIAL PROSTATITIS
- repeated symptoms of UTI with same pathogen grown (may also get pain on ejaculation) (often don’t have fever)
- often norm prostate on DRE (may be tender/enlarged)
= same mx as acute bacterial prostatitis

CHRONIC PELVI PAIN SYNDROME
- bladder irritation symptoms, painful ejaculation, may have bloody semen
- moderate + diffuse pain in perineum, lower back, lower abdo, scrotum, penis
- prostate norm (may be mildly tender)
= anti-inflam analgesia + similar mx to BPH (alpha blockers eg tamsulosin + doxazosin and 5-alphar-reductase inhibitors eg finasteride)

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5
Q

BALANITIS:

  • what is it?
  • big risk factors regardless of cause? 2
A

balanitis = inflammation of the glans penis (ie the bell end)
- can happen in circumcised and non-circumcised men

  • diabetes
  • poor genital hygiene! (build up of smegma)

nb Balanoposthitis is inflammation of both the glans penis and the foreskin

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6
Q

CAUSES OF BALANITIS

  • candidiasis
  • contact / allergic dermatitis
  • dermatitis (eczema or psoriasis)
  • bacterial (+ WHICH PATHOGEN)
  • anaerobic bacterial

FOR EACH

  • how common? (very common, common, uncommon, rare)
  • acute or chronic?
  • how present? incl presence / type of discharge!

nb see other flashcard for other (rarer) causes of balanitis

A

CANDIDIASIS
- very common
- acute
= Usually occurs after intercourse + associated with itching + white non-urethral discharge

CONTACT / ALLERGIC DERMATITIS
- very common
- acute
= Itchy, sometimes painful + occasionally associated with a clear non-urethral discharge. Often there is no other body area affected

DERMATITIS (ECZEMA OR PSORIASIS)
- very common
- acute or chronic
= Very itchy but not associated with any discharge
= will be a PMHx of eczema/psoriasis with active areas elsewhere on body

BACTERIAL
- common
- acute
= Painful and can be itchy with yellow non-urethral discharge
= norm STAPH species

ANAEROBIC BACTERIAL
- common
- acute
= May be itchy but is most associated with a very offensive yellow non-urethral discharge

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7
Q

less common CAUSES OF BALANITIS

  • lichen planus
  • circinate balanaitis
  • lichen sclerosis
  • plasma cell balanitis of Zoon

FOR EACH

  • how common? (very common, common, uncommon, rare)
  • acute or chronic?
  • how present? incl presence / type of discharge!
A

LICHEN PLANUS
- uncommon
- acute or chronic
= May be itchy, the main diagnostic feature is the presence of Wickham’s striae and violaceous papules

CIRCINCATE BALANITIS
- uncommon
- acute or chronic
= Not itchy and not associated with any discharge
= key feature is painless erosions and it can be associated with Reiter’s syndrome (ie reactive arthritis from STI)

LICHEN SCLEROSIS
- aka balanitis xerotica obliterans
- rare
- chronic
= May be itchy, associated with white plaques and can cause significant scarring

PLASMA CELL BALANITIS OF ZOON
- rare
- chronic
= Not itchy with clearly circumscribed areas of inflammation

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8
Q

BALANITIS

  • investigation to do if possible? 1
  • management for all? 1 (regardless of cause)
  • additional mx if severe dicomfort? 1
  • specific treatment dependent on cause? (1 candida, 1 bacterial, 1 anaerobic bacterial, 1 for lichen sclerosis + plasma cell balanitis of zoon)
A

clinical diagnosis

swab any discharge!!

FOR ALL

  • daily retraction of foreskin and warm saline wash
  • 1% hydrocortisone cream (if severe! - only use for short period)

candida = topical CLOTRIMAZOLE (2 weeks)

bacterial = oral fluclox

anaerobic = topical or oral metronidazole

high potency steroids:

  • lichen sclerosis
  • plasma cell balanitis of zoon

use low-potency steroids (eg 1% hydrocortisone) for dermatitis and circinate balanitis

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9
Q

BALANITIS

  • complications? 4
  • possible mx of these?
A
  • post-inflammatory phimosis (may need circumcision)
  • urinary tract obstruction (if siginificant swelling) - will need catheter
  • recurrent UTIs
  • penile cancer (poor genital hygiene is a risk factor!)
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10
Q

PHIMOSIS

  • definition?
  • when is this physiological?
  • additional clinical features? 2
A

PHIMOSIS
= when foreskin can’t be pulled down (retracted) from the tip of the penis

ALL BOYS under 2 have and is normal! - may balloon as they pee - but no prioblem if there’s a miatus!

Physiological if toddler - don’t worry until over age 2 and causing probs (ie recurrent infecitons or other complicaitons!!)

  • painful erection
  • dyspareunia

can also get difficulty in retracting the foreskin (relative phimosis)

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11
Q

PHIMOSIS

  • conservative mx? 2
  • surgical options? 2
  • main complications? 3
A

is a clinical diagnosis!

DON’T FORCE RETRACTION!!!

CONSERVATIVE MX

  • topcial corticosteroid cream (contraindicated if recurrent infection)
  • stretching exercises

SURGICAL MX

  • vertical incision of constricting bands
  • circumcision

COMPLICATIONS:

  • paraphimosis
  • foreskin tear w possible haemorrhage
  • repeated infections! (balanoposthitis)
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12
Q

PARAPHIMOSIS

  • what is it?
  • three main groups of causes?
  • clinical features?
A

PARAPHIMOSIS
= retracted foreskin in an uncircumcised male that cannot be returned to its original position

  • complication of PHIMOSIS
  • IATROGENIC (eg not replacing forseskin after catheterising)
  • TRAUMA (vigerous sex, forceful retraction of foreskin while urinating, piercing)
  • noticeable band of constricting tissue (at the coronal sulcus)
  • Foreskin cannot be returned to its original position
  • Edema and pain of the glans penis
  • features of penile ischemia (blue penile skin and firm glans penis)

PARAPHIMOSIS IS A UROLOGICAL EMERGENCY!!!

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13
Q

PARAPHIMOSIS

  • fully DESCRIBE conservative mx?
  • surgical options? 2
  • complicaiton? 1
A

PARAPHIMOSIS IS A UROLOGICAL EMERGENCY!

conservative = manual reduction of foreskin w adequate analgesia (local or regional block or topical lidocaine) whilst squeezing glans

  • Ice, compression bandages, or gauze soaked in an osmotic agent eg 50% glucose soaked swab (to reduce edema) may assist this process
  • may also need to aspirate blood/fluid from penis to assist

if conservative fails:

  • dorsal slit in foreskin to allow manual reduction
  • circumcision = last resort!

complication = penile necrosis!

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14
Q

ERECTILE DYSFUNCTION:

  • what is it?
  • risk factors for VASCULAR causes? 5
  • NEUROGENIC causes? 5
  • ENDOCRINE causes? 3
  • OHER ORGANIC causes? 3
  • PSYCHOGENIC causes/ risk factors? 5
A

Erectile dysfunction (impotentia coeundi) = inability to achieve or sustain an erection sufficient in rigidity or duration for sexual intercourse which is present for a minimum of ∼ 6 months (although may be treated before this!)

VASCULAR

  • HTN
  • diabetes
  • cardiovascular disease
  • hyperlipidaemia
  • smoking

NEUROGENIC

  • stroke
  • brain or spinal cord injury
  • MS
  • dementia
  • parkinsons

ENDOCRINE

  • hypogonadism
  • hyperprolactinaemia
  • thyroid diseases

OTHER ORGANIC

  • surgery / radiotherapy to region
  • pelvic trauma / fracture
  • alcohol abuse
  • Peyronie disease

PSYCHOGENIC

  • depression
  • anxiety (performace related)
  • relationship issues
  • trauma from prior experiences
  • stress

can get MIXED psychogenic and organic causes!!

increasing AGE is also a risk factor!

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15
Q

Medications that can cause erectile dysfunction? 2

A
  • beta blockers

- SSRIs

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16
Q
ERECTILE DYSFUNCTION:
organic vs psychogenic causes:
- speed of onset of symptoms?
- ability to get an erection?
- libido?
- premature ejaculation?
A

ORGANIC

  • gradual onset
  • can’t get an erection even overnight or when try alone
  • normal libido
  • no hx of premature ejaculation

PSYCHOGENIC

  • sudden onset
  • Good quality spontaneous or self-stimulated erections
  • decreased libido
  • hx of premature ejaculation

also in psychogenic

  • major life events
  • problems or changes in relationship
  • previous psych problems
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17
Q

ERECTILE DYSFUNCTION

  • two tests that should be done by GP to find cause? 2
  • 1st line drug (class and name)? 1 (who is this CI in? 2)
  • 2nd line mx? 1
A
  • QRISK score (for all men presenting w ED)
  • free testosterone measurement (between 9 and 11am)

1st line
= PDE-5 inhibitors (SILDENEFIL - ie viagra)
- prescribe to all (except CI), regardless of cause!
- CI if also taking nitrates or severe postural hypotension)

nb if taking alpha-adrenergic blockers - eg for BPH, take 4hrs apart to prevent hypotension!

2nd line if pt doesn’t want or can’t have sildenafil = VACUUM ASIST DEVICES

nb are other surgical options if those don’t work!

ALSO offer psych support if psychogenic cause!

NB for a young man who has always had difficulty achieving an erection, referral to urology is appropriate

NB people with erectile dysfunction who cycle for more than three hours per week should be advised to stop

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18
Q

EPIDIDYMO-ORCHITIS

  • what is it?
  • two main causes, incl specific pathogen? 2 (who gets which? 2)
A

inflammation of epididymis and testicles (norm as reulst of infection)

< 35 years
= norm STI
- chlamydia, gonorrhoea or rarer ones

> 35 years (or children)
= norm UTI
- E.coli (or rarely pseudomonas or other STIs)

nb can get chronic infection - but rare and often TB or weird thing like amiodarone-induced or autoimmune diseases

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19
Q

EPIDIDYMO-ORCHITIS:

- describe clinical presentation? (incl signs + symptoms)

A

Unilateral scrotal pain and swelling
- develops over several days and radiates to the ipsilateral flank

Tenderness along the posterior testis

Scrotal skin overlying the epididymis may appear red, shiny, and edematous

Low-grade fever (especially among children)

Symptoms of lower urinary tract infection (e.g., dysuria, frequency, urgency), including urethritis (urethral discharge)

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20
Q

EPIDIDYMO-ORCHITIS:

  • main DDx to rule out?
  • clincial test (incl name) to rule out?
  • other symptoms/features which make DDx more likely? 3
A

need to rule out testicular torsion

PREHN SIGN
= elevation of the scrotum reduces testicular pain
- positive = epidydimo-orchitis
- negative (ie pain not relieved) = torsion

other signs suggestive of torsion:

  • patients < 20 years
  • severe pain
  • acute onset

nb you can also get torsion of the epididymal appendices (more localised pain / swelling than full torsion)

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21
Q

EPIDIDYMO-ORCHITIS:

  • bedside tests to consider? 4
  • imaging? 1 (when is it indicated? 2)
A

if UTI suspected

  • urine dip
  • MSU

if STI suspected

  • urethral NAAT swab
  • urethral swab for culture

scrotal USS if:

  • can’t rule out testicular torsion based on hx + physical
  • if suspect an abscess
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22
Q

EPIDIDYMO-ORCHITIS:

  • management if suspected UTI cause?
  • management if suspect STI cause? 2 (name specific drugs)
  • symptomatic management? 3
A

UTI cause
- fluoroquinolones (eg levofloxacin)

STI cause
- ceftriaxone IM single dose PLUS doxycycline PO for 10-14 days

  • NSAIDs
  • scrotal elevation
  • icepacks (be careful!)
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23
Q

TESTICULAR CANCER

  • peak age group?
  • commonest type of tumour?
  • risk factors? 6
A

20-35 years

germ cell tumours (95%)

  • seminomas (40%)
  • non-seminomas (rest)(embryonal, yolk sac, teratoma and choriocarcinoma)

RISK FACTORS

  • cryptorchidism (undescended testes)
  • infertility
  • mumps orchitis
  • klinefelter syndrome
  • trisomy 21
  • FHx testicular Ca (also PMHx)

see amboss for all the slightly different types of germ cell tumours

nb if get lump in testes in man over 60 then likely to be lymphoma!

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24
Q

TESTICULAR CANCER

  • most common presenting symptom? 1
  • other possible symptoms? 3
A

painless lump in testicles

  • pain (sometimes)
  • hydrocele
  • gynaecomastia
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25
Q

TESTICULAR CANCER

  • 1st line imaging? 1
  • additional imaging needed? 2
  • tumour markers to do? 3
  • which tumour markers are raised in which sub-type?
A

1st) ULTRASOUND
- do NOT do trans-scrotal biopsy! - can cause spread!!

CT of abdo pelvis + norm chest too for stagting (as can spread a lot!)

1) AFP
- always high in: yolk sac (F is for Foetal - ie in a yolk sac!)
- may be high in: mixed germ cell

2) HCG
- always high in: choriocarcinoma (C for Chorio)
- may be high in: mixed germ cell

3) LDH
- non-specific marker of cell turnover (lactate dehydrogenase)
- marker of prognosis (response to Tx) and detects relapse i.e. metastatic disease

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26
Q

TESTICULAR CANCER

  • where do they metastasise to first?
  • what to do BEFORE treatment? 1
  • main treatment? 1
  • other treatments that may be offered? 1
A

metastasise to PARA-AORTIC lymph nodes (these are retroperitoneal)

Prior to surgery: sperm cryopreservation

RADICAL INGUINAL ORCHIECTOMY (ie pull out through inguinal canal - to avoid haem spread)

if stage I (confined to testes, no lymph node spread) then can do active surveillence but most get chemo and/or radio too - and all that have spread to lymph nodes (stage II) or distant mets (stage III) get chemo!

testicular tumours are very chemo responsive and is about 95% cure rate!

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27
Q

BREAST FIBROADENOMA

  • characteristics?
  • age norm seen in?
  • investigations? 3
  • prognosis?
  • management if large?
A

nb most common breast lesion!

Mobile, firm breast lumps - a ‘breast mouse’
- doesn’t getr bigger/smaller with periods, no pain!

age 20-40

triple assessment!
- exam, USS (under 40) or mammogram (over 40) and core needle biopsy

NO CANCER RISK! (except see below)
- 1/3 regress, 1/3 stay same, 1/3 enlarge

if over 3cm then tend to surgically remove!

nb rarely can get
Complex Fibroadenomas
- Moderately differentiated cells
- Slight ↑risk of Ca

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28
Q

MASTITIS

  • what is it?
  • who almost exclusively seen in? 1
  • additional risk factors? 3
  • most common causative organism?
A

inflammation of the breast parenchyma

occurs in up to 10% of BREASTFEEDING mothers (particularly 2–4 weeks postpartum)

anything that causes insufficient drainage of milk -> milk stasis:

  • infrequent feeding
  • quick weaning
  • illness in either mother or baby

norm STAPH AUREUS

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29
Q

MASTITIS

  • local symptoms? 3
  • possible systemic symptoms? 3
A
  • Tender, firm, swollen, erythematous breast (generally unilateral)
  • Pain during breastfeeding
  • Reduced milk secretion

flu-like symptoms

  • malaise
  • fever
  • chills

is a clinical diagnosis!

can get reactive lymphadenopathy

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30
Q

MASTITIS

  • 1st line management? 1
  • symptomatic relief? 2
  • indications for Abx? 3 (which abx?)
  • possible complciation? 1
A
CONTINUE BREASTFEEDING (baby already has the bug!)
- if can't then use breast pump but breastfeeding better!
  • NSAIDs (fine for breastfeeding)
  • cold comresses

fluclox 10-14 days if:

  • systemically unwell
  • nipple fissure present
  • symptoms don’t improve after 24hrs of effective milk removal

^keep breastfeeding while have abx!

can develop a BREAST ABSCESS (norm if they stop breast feeding)

nb if inadequate response to treatment, do breast milk cultures

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31
Q

BREAST ABSCESS

  • how presents? (describe the mass and other symptoms)
  • management? 2
A

complicaiton of mastitis

a TENDER, FLUCTUANT mass

  • Breast pain, erythema, and oedema
  • Purulent discharge from the nipple of the affected breast
  • Fever
  • nausea

mx

  • antibiotics
  • incision + drainage!

nb Overlying skin necrosis is an indication for surgical debridement, which may be complicated by the development of a subsequent mammary duct fistula

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32
Q

FAT NECROSIS OF BREAST

  • peak age incidence?
  • other risk factor? 1
  • cause? 1
  • pathophysiology?
  • what it feels like?
  • investigations? 3
A

around 50

typically obese women with large breasts

trauma (although many women don’t report any or it may be very minor trauma!)

Initial inflammatory response, the lesion is typical firm and round but may develop into a hard, irregular breast lump

  • norm painless
  • may get associated skin and nipple changes

triple assessment

  • clinical exam
  • imaging
  • core biopsy

is rare and often presents very similar to breast Ca so always fully investigate!

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33
Q

FIBROCYSTIC DISEASE:

  • aka? 2
  • what is it?
  • typical age affected?
  • clinical presentation?
  • 1st line management? 1
  • management if persistent or affecting ADLs? 1
A
  • aka fibroadenosis
  • aka benign mammary dysplasia

benign changes characterised by the formation of fibrotic and/or cystic tissue

middle aged pre-menopausal women

  • Premenstrual bilateral multifocal breast pain
  • Tender or nontender breast nodules
  • may have Clear or slightly milky nipple discharge

Mx = Mainly supportive with analgesia for pain control

Hormone therapy can be considered for those with >6m symptoms of severe breast pain + impact on ADLs. These treatments are infrequently used bc of adverse effects.

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34
Q

CAUSES OF NIPPLE DISCHARGE:

describe presentation + cause of each:

  • physiological?
  • galactorrhoea?
  • hyperprolactinaemia?
  • intraductal papilloma?
  • mammary duct ectasia?
  • carcinoma?

also what driugs can cause high prolactin?

A

PHYSIOLOGICAL

  • during breast feeding
  • can also get a bit during pregnancy

GALACTORRHOEA
- Commonest cause may be response to emotional events, drugs such as histamine receptor antagonists are also implicated (can also get in end-stage kidney disease)

HYPERPROLACTINAEMIA

  • Commonest type of pituitary tumour
  • – Microadenomas <1cm in diameter
  • – Macroadenomas >1cm in diameter
  • Pressure on optic chiasm may cause bitemporal hemianopia

INTRADUCTAL PAPILLOMA

  • Commoner in younger patients but also middle-aged women!
  • May cause blood stained discharge
  • There is usually no palpable lump

MAMMARY DUCT ECTASIA

  • Dilatation breast ducts.
  • Most common in menopausal women
  • Discharge typically thick and green in colour
  • Most common in smokers

CARCINOMA

  • Often blood stained
  • May be underlying mass or axillary lymphadenopathy

any antidopaminergic drugs

  • metoclopramide
  • 1st gen (and 2nd gen) antipsychotics
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35
Q

NIPPLE DISCHARGE

  • first line investigation to do if galactorrhoea (ie milky discharge from both nipples)?
  • bedside test for all? 1
  • if this is high, what further simple tests could you do? 3
  • if all these further tests are negative, what imaging to do? 1
A

measure PROLACTIN

if not high, no pathological cause for galactorrhoea

do VISUAL FIELD test (looking for bitemporal hemianopia)

if elevated do:

  • TSH (primary hypothyroidism)
  • bHCG (pregnancy)
  • creatinine (chronic kiney disease)

^if these three tests are normal and priolactin is high: do MRI of head (to look for pituatory adenoma)

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36
Q

NIPPLE DISCHARGE

  • investigation if discharge is one-sided OR non-milky? 3
  • if this comes back negative? 1
A

send for triple assessment - incl biopsy

if this negative: measure prolactin and then see previous flashcard for other investigations!

nb signs that suggest malignancy:

  • Spontaneous, unilateral, uniductal, and bloody discharge
  • Presence of a breast mass or abnormalities in imaging
  • Age > 40 years
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37
Q

management of causes of nipple discharge

  • galactorrhoea?
  • intraductal papilloma?
  • mammary duct ectasia?
  • carcinoma?

nb see endocrinology cards for mx of prolactin secreting tumours

A

if bilateral galactorrhoea with NORMAL prolactin and non lump then can reassure!

intraductal papilloma:
- if troubling can have: microdochectomy (if young) or total duct excision (if older)

mammary duct ectasia
- smoking cessation advice
- mx usually not needed
- if troubling can have: microdochectomy (if young) or total duct excision (if older)
(nb may progress to breast abscess)
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38
Q

BREAST LUMP DDx

briefly describe how each of these would present / a little about them

  • fibroadenoma
  • fibrocystic changes / fibroadenosis
  • breast cysts
  • phyllodes tumour
  • fat necrosis
  • galactocele
  • intraductal papilloma
  • mammary duct ectasia
  • breast cancer
A

FIBRADENOMA
- Solitary, well-defined, non-tender, rubbery, and mobile mass

FIBROCYSTIC CHANGES

  • Premenstrual breast tenderness
  • Multiple breast nodules bilaterally

BREAST CYSTS

  • well circumscribed (may feel like a grape, or water-balloon in the breast)
  • usually firm but not hard, and mobile
  • may get larger and smaller depending on stage of menstrual cycle

PHYLLODES TUMOUR

  • Painless, smooth, multinodular lump
  • Variable growth rate
  • Generally > 3 cm
  • needs surgical excision!

FAT NECROSIS

  • Irregularly defined and dense periareolar breast mass
  • Skin retraction, erythema, and ecchymosis

GALACTOCELE

  • Painless, firm mass
  • most common lesion in breast feeding women

INTRADUCTAL PAPILLOMA

  • Solitary lesions
  • Bloody nipple discharge
  • Palpable breast lump close to or behind the nipple
  • nb Multiple lesion are usually asymptomatic

MAMMARY DUCT ECTASIA

  • Unilateral greenish or bloody discharge
  • Nipple inversion
  • Firm, stable, painful mass under the nipple

BREAST CANCER

  • hard, painless (90%), irregular margins, fixed to skin or chest wall
  • skin dimpling may occur, may have unilateral nipple discharge +/or nipple retraction
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39
Q

BREAST LUMP REFERRAL:

  • criteria for 2WW? 2
  • consider 2WW? 2
  • criteria for non-urgent referral? 1
A

2WW

1) aged 30 years or more
- unexplained breast lump (with or without pain)

2) aged 50 or more
- UNILATERAL discharge, retraction, any other nipple changes

also consider 2WW for:

  • pt w skin changes that suggest breast cancer
  • 30 years and over with an unexplained lump in the axilla

non-urgent referral:
- under 30 with unexplained breast lump

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40
Q

PAINLESS TESTICULLAR SWELLING DDx

briefly describe how each of these would present / a little about them
- AND finding on ultrasound (+ whether transilluminate)

  • hydrocele
  • spermatocele
  • varicocele
  • scrotal hernia
  • testicular tumour
A
HYDROCELE
- Fluctuant swelling of the scrotum
- transilluminates
- nb MAY be presenting feature of testicular Ca!
= Hypoechoic mass around the testis

SPERMATOCELE
= aka EPIDIDYMAL CYSTS
- Fluctuant swelling of the upper testicular pole
- transilluminates
= Hypoechoic dilation of epididymal duct or rete testis

^ie hydrocele is fluid surrounding testes, spermatocele is fluid filled sac on top iof epididymis

VARICOCELE
- Usually painless (can be a dull pain) swelling may be reduced when supine
- norm on Left (may be 1st presentation of renal Ca)
- Visible or palpable strands and “bag of worms” sensation
- bilateral varicoceles may affect fertility
- doesn’t transilluminate
= Dilated hypoechoic pampiniform vessels

SCROTAL HERNIA
- can't get above it on exam!
- cough impulse may be present + may be reducible
- doesn't transilluminate
= Herniated bowels on USS
TESTICULAR TUMOUR
- Usually painless mass (however, may feel dull ache or "heavy" sensation in the testicle)
- Palpation of solid mass
- doesn't transilluminate
= Solid mass with variable echogenicity
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41
Q

PAINFUL TESTICULAR SWELLING / TESTICULAR PAIN DDx

for each, briefly describe:

  • hx
  • exam findings
  • blood / urine dip results
  • testicular torsion
  • acute epididymo-orchitis
  • torsion of testicular appendage
  • testicular tumour
A

TESTICULAR TORSION
- Sudden onset unilateral painful testis/lower abdomen w nausea or vomiting
- Swollen, edematous, tender testis
- Abnormal position of testis (e.g., transverse lie, scrotal elevation)
- Negative Prehn sign (elevating testicles doesn’t relieve pain)
- Absent cremasteric reflex
= normal inflam markers + urine dip

ACUTE EPIDIDYMO-ORCHITIS
- onset over a few days, painful swelling with possible induration
- possible history of urethral discharge, fever, dysuria, urinary freq
- Very tender (physical examination is painful)
- Positive Prehn sign
- Positive cremasteric reflex
= increase in inflamm markers, possible pyuria on urine dip/MSU

TORSION OF TESTICULAR APPENDAGE
- Insidious onset of unilateral scrotal pain
- Usually seen in boys 3–5 years of age
- Tender testis
May manifest with blue dot sign
= typically norm inflamm markers and urine dip

TESTICULAR TUMOUR
- Slow progression (e.g., weeks to months)
Usually painless mass (however, the patient may experience a dull ache or describe a “heavy” sensation in the testis)
- Easy palpation of solid mass
- Possible manifestations of metastatic disease (e.g., distant lymphadenopathy, chest pain, GI symptoms)
- Possible swelling of the ipsilateral lower limb (venous engorgement due to obstruction)
= possible increase in serum tumour markers: AFP, HCG, LDH

also STRANGIULATED INGUINAL hernia

can also get HAEMATOCELE (following acute trauma)

  • admit if acute!
  • if it is chronic or does not follow trauma - refer as out patient USS! - still need to be seen!
42
Q

1st line investigation for any testicular / scrotal mass? 1

A

USS scrotum

nb if high suspision of testicular torsion - just go straight to surgery!

DON’T biopsy trough scrotum!!

43
Q

Mx of some testicular masses:

  • torsion of testicular appendage
  • hydrocele
  • spermatocele
  • varicocele
  • scrotal hernia
A

TORSION OF TESTICULAR APPENDAGE

  • NSAIDs for pain, can be maged conservatively
  • may need surgical exploration

HYDROCELE

  • Hydrocele should be managed depending on whether it is congenital or non-congenital, as well as the size of the hydrocele
  • always needs USS to see if underlying Ca!

SPERMATOCELE

  • aka EPIDIDYMAL CYSTS
  • should be reassured, as they rarely need treatment

VARICOCELE

  • norm managed conservatively
  • If concerns about infertility then surgery or radiological mx can be considered

SCROTAL HERNIA

  • if strangulated or causing obstruction - admit immediately
  • if not, refer in 2 weeks for infant or young boy!
  • refer for elective surgery for men or older boys
44
Q

HYPERVENTILATION / PANIC ATTACK

  • symptoms? 12 (incl 2 from low CO2)
  • signs? 3
  • how long normally last?
A

Panic attack is excessive fear without an obvious trigger; associated with symptoms of autonomic arousal:

  • sweating
  • tremors
  • tingling fingers
  • periorbital tingling
  • dizziness
  • nausea
  • palpitations
  • tight chest / chest pain
  • breathlessness
  • worry
  • irritability
  • fear
  • derealisation

= tremor
= high HR
= high RR

usually lasts < 30 mins

45
Q

HYPERVENTILATION / PANIC ATTACK

  • investigations to consider to rule out organic causes?
  • what find on a blood gas?
  • acute management? 3
  • long-term management? 3
A

Basically think about the differentials for SOB and chest pain (and match with risk factors, incl age)

will NOT do all of these but may do some of:

  • ECG
  • troponin
  • FBC
  • TFTs
  • glucose

if blood gas: resp alkalosis (low CO2)

ACUTE Mx

1) Breathe into paper bag if hyperventilating (increases CO2 uptake to manage symptoms)
2) Careful explanation of what is happening, that they wont pass out, and explore what is causing it
3) short-acting benzo (eg lorazepam) if really struggling

if repeated (panic disorder), go to GP, for:

  • CBT
  • antidepressants
  • propranolol (pill in pocket)

additional ?helpful advice:

  • Breathing exercises (silently counting up to 10)
  • Visualisation techniques (imagine colour/place)
  • Relaxation music
  • Yoga
46
Q

ACUTE BRONCHITIS:

  • describe pathophysiology?
  • normal causative organism?
A

a self-limiting lower respiratory tract infection (RTI) characterized by inflammation of the bronchi

> 90% are caused by viruses

Influenza A and B
Parainfluenza
Adenovirus
RSV
Rhinovirus
Coronavirus
47
Q

ACUTE BRONCHITIS

  • norm preceeded by? (2 main symptoms)
  • describe cough? (incl duration)
  • other symptoms? 5
  • uncommon symptom? 1
A

norm preceeded by an URTI

  • runny nose
  • sore throat

COUGH

  • > 5days (resolves in 2-3 wks)
  • sputum (50%) (purulence doesn’t always mean bacterial cause!)
  • chest pain
  • SOB
  • headache
  • myalgia
  • malaise

fever (uncommon) - if fever, likely dt influenza (or actually pneumonia!)

48
Q

ACUTE BRONCHITIS

  • how diagnosis made?
  • what may find on auscultation?
  • management? 2
  • prognosis?
  • main complication? 1
  • patient groups at risk of complciations? 3
A

nb if in small child - think bronchiolitis!

clinical diagnosis

may get a bit of wheezing on auscultation (but ?may also get crackles?? - check this!!**)

  • rest + adequate hydration (promotes mucus secretion)
  • simple analgesia for myalgia/headache

antibiotic not recommended!!!

generally self-limiting

main complicaiton = secondary bacterial infection, ie pneumonia

at risk for complications:

  • elderly
  • pre-existing lung conditions
  • immunocompromised
49
Q

DDx of ACUTE COUGH

  • non-life threatening? 2
  • potentially life-threatening? 5
A

ie cough < 3 weeks in adults!

  • upper resp tract infections
  • acute bronchitis
  • pneumonia
  • acute exacerbation of asthma/COPD
  • acute PE
  • congestive heart failure
  • acute inhalational injury (eg smoke or chemicals)

nb acute pericarditis can rarely have a cough

ALSO COVID! how could I forget?

50
Q

SPONTANEOUS PNEUMOTHORAX

  • difference between primary and secondary?
  • two other causes of non-spontaneous pneumothoraces?
A

Primary (PSP)
= patient has NO underlying lung pathology (on Hx, exam or CXR) - norm tall young men

Secondary (SSP)
= patient has underlying lung pathology (COPD, asthma, pneumonia, Ca, TB, fibrosis etc)

NON-SPONTANEOUS

  • iatrogenic ( eg secondary to pleural aspiration, +ve pressure ventilation)
  • trauma (eg rib #)
51
Q

RED FLAGS for TENSION PNEUMOTHORAX? 8

A
  • Very high RR
  • ↑HR
  • ↓BP
  • resp distress
  • distended neck veins
  • cyanosis
  • agitation
  • tracheal deviation (late)

basically if someone with symptoms/signs of a pneumothorax becomes HAEMODYNAMICALLY UNSTABLE

52
Q

PNEUMOTHORAX

  • 1st line investigation? (be specific)
  • definition of large and small? (by cm)
  • other investigation that can rarely be used? 1
  • WHEN MANAGE IMMEDIATELY? 2 (and how)
A

1st line:
= ERECT chest X-ray
- Hypodense area with loss of vascular markings, can see lung edge

  • Small < 2cm
  • Large > 2cm

Should never order if tension (would see mediastinal shift)

also do bloods depending on clinical picture, incl ABG if hypoxic

2nd line: CT scan - if uncertainty on CXR or complex case

MANAGE URGENTLY IF:

  • tension
  • bilateral

give:

  • high flow O2
  • needle decompression AND urgent chest drain!
53
Q

Management of PRIMARY SPONTANEOUS PNEUMOTHORAX:

  • if < 2cm AND not SOB? 1
  • if >2cm and/OR SOB? 2

Additional advice for all? 1

A

PRIMARY spontaneous pneumothorax (PSP)

If size < 2cm and not SOB:
- consider discharge (review in OPD in 2-4wks)

If size > 2cm and/or SOB:

  • Aspirate with cannula
  • – If success: consider discharge (see above)
  • – If no success: chest drain (& admit)

TREAT primary based on SHORTNESS OF BREATH, not size!

If discharge, safety net to come back if get SOB (& NO FLYING until full resolution)

54
Q

Management of SECONDARY SPONTANEOUS PNEUMOTHORAX:

  • If size < 1cm and not SOB? 2
  • If size 1-2cm and not SOB? 2
  • If size > 2cm and/or SOB? 2

if chest drain in, what to do before take it out?

when to call thoracic surgeons? 1

A

this is for SECONDARY - ie have underlying lung disease (either on Hx, exam or test results - eg chronic CO2 retainer)

If size < 1cm and not SOB:

1) High-flow oxygen (unless retain CO2!)
2) Observe for 24hrs

If size 1-2cm and not SOB:

1) Aspirate with cannula
- – If success (ie <1cm): High flow O2 and 24hr observe (see above)
- – If no success: chest drain (& admit)

If size > 2cm and/or SOB:
1) chest drain (& admit)

always re-CXR before removing chest drain to check fully resolved!

consult surgeons if:
- persistent air leak or failure of lung to re-expand with drain at 3-5 days

55
Q

Management options if recurrent pneumothoraces? 2

A

1) Surgery to remove bullae / diseased lung

2) Pleurodesis (if not fit / don’t want surgery)

56
Q

PLEURAL EFFUSION

  • difference between transudates and exudates? (incl pathophysiology)
  • which more likely to be unilateral + bilateral?
A

as a general rule pleural effusions form as a result of increased fluid formation and/or reduced fluid reabsorption

TRANSUDATES

  • Think ↑Venous pressure and/or Hypoproteinaemia!
  • More likely to be BILATERAL

EXUDATES

  • Think infection, inflammation, infarction or malignancy!
  • More likely to be UNILATERAL
57
Q

CAUSES of PLEURAL EFFUSIONS:

  • transudates (2 most common, 5 rarer)
  • exudates (3 most common, 6 rarer)
A

TRANSUDATES

= LEFT ventricular failure
= liver cirrhosis

  • Hypoalbuminaemia
  • Peritoneal dialysis
  • Hypothyroidism
  • Nephrotic syndrome
  • Mitral stenosis

nb other rarer causes of transudates: Constrictive pericarditis, Urinothorax, Meigs’ syndrome

EXUDATES

= Malignancy
= Parapneumonic effusions
= Tuberculosis

  • PE
  • Pancreatitis
  • Rheumatoid arthritis (+ other autoimmune pleuritis)
  • Benign asbestos effusion
  • Post-myocardial infarction
  • Post-coronary artery bypass graft

nb other rarer causes of exudates: Yellow nail syndrome (& other lymphatic disorders), Some medications, Fungal infections

58
Q

PLEURAL EFFUSION:

  • typical Hx?
  • typical findings on auscultation + percussion? 2
  • red flags for malignancy? (4 symptoms, 2 RFs)
A

Typical Hx:

  • Progressive dyspnoea (days-wks)
  • pleuritic chest pain
  • cough

Typical exam findings:

  • Stony dull (percussion)
  • reduced breath sounds (auscultation)

Malignancy red flags:

  • Weight loss
  • anorexia
  • fatigue
  • haemoptysis
  • smoker (or ex)
  • asbestos exposure
59
Q

PLEURAL EFFUSION

  • 1st line investigation? (how much fluid needs to be there for this investigation to pick it up?)
  • 2nd line investigation? (when don’t you need this? what is tested in it?)
  • how do you differentiate between transudate and exudate?
A

1st line:
= CXR
- Opacity at base of lung with meniscus / blunting of costophrenic angle(s)

need >200ml on PA or >50ml on Lateral to be visible (‘normal’ x-ray doesn’t exclude effusion!)

If likely transudate from clinical presentation & CXR, treat this (ie don’t need to do aspiration)

2nd line:
= US-guided pleural aspiration AND bloods

pleural USS can visualise septations (indicating exudate) and can pick up smaller effusions than CXR

Look at & smell aspirate (putrid odour, milky, bloody, ‘anchovy sauce’)

Tests for ALL pleural aspirates:
= LDH & protein (for Light’s criteria)
= Microscopy & culture
= Cytology (malignant & immune cells)

Bloods:
= LDH and Total protein (Light’s criteria)
= PLUS others to find cause eg FBC, LFTs

nb Other aspirate tests if high clinical suspicion:

  • pH (infection)
  • Glucose (low = likely rheumatoid)
  • TB culture
  • Triglycerides & cholesterol (chylothorax)
  • Amylase (pancreatitis)
  • Haematocrit (haemothorax)

LIGHT’S CRITERIA
- distinguish between exudate & transudate

= Ratios between protein and LDH in serum vs pleural fluid

Specific values but simply: INCREASED protein and LDH in pleural fluid = likely exudate

Nb 3rd line: CT scan - to distinguish between malignant & benign causes of exudate (if aspiration not definitive)

60
Q

PLEURAL EFFUSION

  • management options? 1 acute, 2 recurrent (ie of the actual effusion)
  • what else need to treat? 1
A

TREAT EFFUSION

1st) chest drain (if exudate)

if recurrent:

  • long-standing drain (managed by district nurses)
  • pleurodesis (tetracycline, bleomycin or sterile talc)

TREAT UNDERLYING CAUSE
- eg chemo for cancer, diuretics for HF

for transudate: norm just treat underlying cause and this will treat!

61
Q

PARANEOPLASTIC syndromes associated with LUNG CANCERS:

  • small cell? 3
  • squamous cell? 3
  • adenocarcinoma? 2

ALL lung Ca? 2 haem, 2 derm

briefly describe ones that aren’t obvious

LEARN THESE! - OFTEN COME UP IN EXAMS!

A

SMALL CELL

  • SIADH (syndrome of inappropriate anti-diuretic hormone)
  • CUSHINGS (ectopic ACTH)
  • LAMBERT-EATON syndrome

“when you’re SMALL: you PEE a lot, you’re CHUBBY and your MUSCLES don’t work that well”

lambert-eaton = antibodies against presynaptic calcium channels in NMJ -> weakness that improves with repetitive stimulation (similar to myasthenia gravis)

nb cushings due to lung ca is not typical: HTN, high glucose, low K, alkalosis are more common than buffalo hump etc

SQUAMOUS CELL

  • parathyroid hormone-related protein (PTH-rp) secretion -> HYPERCALCAEMIA
  • hypertrophic pulmonary OSTEOARTHROPATHY (HPOA)
  • HYPERTHYROIDISM (dt ectopic TSH)

HPOA = clubbing and painful joint swelling (periostitis)
- can also get in adeno!

“In QUebec they get more bone probs = HIGH CALCIUM + CLUBBING - also GOITERS”

ADENOCARCINOMA

  • THROMBOPHLEBITIS MIGRANS (aka Trousseau syndrome)
  • GYNAECOMASTIA (also large cell)

“ADenocarcinoma ADDS BREAST tissue to men, and ADDs VEINS everywhere too!”

nb Thrombophlebitis migrans is also associated with pancreatic adenocarcinoma

ALL LUNG CA:

  • Thrombocytosis + DIC
  • Hypercoagulability (higher risk in adeno)
  • Dermatomyositis
  • Acanthosis nigricans
62
Q

Describe the symptoms / features that occur when lung cancers infiltrate / compress these structures:

  • superior vena cava?
  • recurrent laryngeal nerve?
  • phrenic nerve?
  • another area of the lung?
  • oesophagus?
A

SUPERIOR VENA CAVA
- SVC syndrome (see oncological emergencies)

RECURRENT LARYNGEAL NERVE (esp pancoast tumours)
- hoarse voice

PHRENIC NEVRE

  • dyspnoea
  • diaphramatic elevation

ANOTHER BIT OF LUNG

  • lobe/lung collapse
  • postobstructive pneumonia

OESOPHAGIUS
- dysphagia

recurrent respiratory infections (e.g. pneumonia) in the same pulmonary region in patients ≥ 40 years old should always raise suspicion for lung cancer!

nb pancoast are nonrm NSCLC:

  • Horner’s synd. – miosis (anisocoria), anhidrosis, ptosis
  • Pancoast’s synd. – pain in nerve root distribution
63
Q

METASTATIC LUNG CANCER

  • what % of pts have metastases at presentation?
  • where are the 4 places that normally metastasise to? 4 (nb excluding the other lung…) (how to remember?)

describe how each of these would presnet?

A

over 50% have metastatic disease at the time of presentation

BLAB!
- “lung cancers like to blab!

BRAIN

  • headache (raised ICP features)
  • seizures
  • focal motor deficits
  • behavioural changes

LIVER

  • typically asymptomatic
  • may manifest with nausea, jaundice, ascites

ADRENAL GLANDS
- typically asymptomatic

BONES

  • bone pain
  • elevated serum alkaline phosphatase (ALP) and calcium

Bone mets in Lung Ca are LYTIC!!

64
Q

SARCOIDOSIS

  • pathophysiology? (be PSECIFIC)
  • age and gender most affected?
  • other main risk factor?
  • two different types? 2
A

a mulit-system disorder characterised by widespread, immune-mediated formation of NON-CASEATING GRANULOMAs

nb cause or underlying pathology is not known!

  • female (2:1)
  • 25-35 years old (2nd peak at: 50-65)

10 TIMES higher in black ethnicity (compared to white)

  • acute (1/3rd)
  • chronic (2/3rds)

^acute only rarely develops into chronic! (chronic norm develops without acute!)

65
Q

ACUTE SARCOIDOSIS

  • speed of onset?
  • systemic symptoms? 4
  • pulmonary symptoms? 3
  • extra-pulmonary symptoms? 3
A

Typically has a sudden onset and remits spontaneously within approx. 2 years

Progression to chronic sarcoidosis is rare

  • fever
  • malaise
  • lack of appetite
  • weight loss

PULM

  • SOB
  • cough
  • chest pain

EXTRA PULM

  • arthritis
  • anterior uveitis
  • erythema nodosum
66
Q

CHRONIC SARCOIDOSIS

  • speed of onset?
  • pulmonary symptoms? 2
  • three most common groups of extra-pulmonary symptoms? 3
  • briefly list other possible manifestations?

acronym to remember different features?

A

Gradual disease course; may be recurrent or progressive
- can rarely be preceeded by acute sarcoidosis

often ASYMPTOMATIC in early stages
- can be picked up on CXR as incidental finding!

PULM (most common)

  • interstital fibrosis
  • – cough
  • – SOB

ENLARGED LYMPH NODES (40%)
- in 90% found within thorax (ie mediastinum)

OCULAR (25%)

  • Granulomatous uveitis (norm anterior, can be posterior)
  • if sarcoidosis diagnosed: see opthalmologist to exclude this!!

SKIN FINDINGS (25%)

  • lupus pernio
  • facial rash, similar to lupus
  • scar sarcoidosis (inflamed, purple skin infiltration and elevation of old scars or tattoos)

lupus pernio = pathognomic for sarcoidosis

  • extensive, purple skin lesions (violaceous skin plaques) on the nose, cheeks, chin, and/or ears
  • aka epithelioid granulomas of the dermis

nb sarcoidosis can affect ANY organ!

OTHER MANIFESTATIONS (don’t worry about learning all!)

  • MSK (arthritis similar to RA, bone lesions)
  • NEURO (CN palsy - facial most common, diabetes insipidus, meningitis, hypopit)
  • HEART (restrictive cardiomyopathy, pericardial effusion, AV block, sudden cardiac death)
  • LIVER (hepatic granulomas, hepatomegaly in 30% of cases)
  • KIDNEYS (norm related to calcium metabolism - eg nephrocalcinosis, nephrolithiasis)
  • SPLEEN (splenomegaly in 30%)

Features of sarcoidosis are GRUELING:

  • Granulomas
  • aRthritis
  • Uveitis
  • Erythema nodosum
  • Lymphadenopathy
  • Interstitial fibrosis
  • Negative TB test
  • Gammaglobulinemia
67
Q

SARCOIDOSIS:

  • 1st line investigation if suspect acute OR chronic? 1 (findings?)
  • gold standard diagnostic test? 1 (incl finding)
  • bloods raised in acute and chronic? 1
  • additional bloods which will likely be increased in CHRONIC sarcoidosis? 2
A

1st) CXR
- Bilateral hilar lymphadenopathy
+/- Bilateral reticular or ground-glass opacities

there is a staging system (based on CXR) for chronic sarcoidosis from normal -> fibrosis

nb pts with chronic sarcoidosis often have moderate clinical manifestations but radiographic findings of extensive disease

gold standard = BRONCHOSCOPY with BIOPSY of lung + lymph nodes

  • NON-CASEATING GRANULOMAS with GIANT cells (central necrosis is absent)
  • ASTEROID bodies, SCHAUMANN bodies

INFLAMMATORY markers - raised in acute + chronic (CRP + ESR)
- can also get lymphopenia (low WCC)

raised in CHRONIC:

  • ACE (angiotensin coverting enzyme) raised in 60% (used for monitoring disease progression)
  • high CALCIUM (10%)

ALP is raised if liver involvement!

nb IgG is also raised in 50% of pts but ?rarely tested for

nb can do CT scan if CXR not clear / to rule out differentials!

nb can get restrictive or obstructive patterns on spirometry

68
Q

SARCOIDOSIS

  • 1st line management? 1
  • indications for giving this? 3
  • additional management options?
A

Isolated pulmonary sarcoidosis: In most cases, no treatment is required. The disease is often asymptomatic, non‑progressive, and has a high rate of spontaneous remission

1st) CORTICOSTEROIDS
indications:
- CXR stage 2 or 3 disease who are symptomatic 
- hypercalcaemia
- eye, heart or neuro involvement

nb asymptomatic and stable stage 2 or 3 disease who have only mildly abnormal lung function do not require treatment

can use NSAIDs for symptom relief!!

if bad, can use:

  • methotrexate
  • azathioprine
  • chloroquinine / hydroxychloroquinine

lung transplant is last resort!

69
Q

long-term COMPLICATIONS of SARCOIDOSIS

  • malignancy? 2
  • pulmonary? 2
  • other? 1
A

norm only get major complications with stage 3 or 4!

  • lung cancer
  • malignant lymphomas
  • brochiectasis
  • lung fibrosis
  • chronic renal failure (esp in pts w hypercalcaemia)
70
Q

TUBERCULOSIS

  • causative organism?
  • how spread?
  • describe pathogenesis?
  • TB infection vs TB disease?
  • latent TB vs active disease?
  • what is milliary TB?
A

mycobacterium tuberculosis (also rarely: m. bovis + m. africanum)

Spread via resp droplets (only pulm version is infectious)

TB infection vs TB disease

  • 90% of those infected, TB is dealt with effectively by immune system without symptoms
  • 10% will go on to develop into TB disease at some point – usually within 1-2 years

Latent TB vs active disease

  • Latent TB occurs due to granuloma formation around the infection ‘sealing’ it off, asymptomatic
  • Active disease occurs when then elderly, malnourished or immunocompromised etc and re-activates

Mycobacteria reach lung alveoli and get engulfed by macrophages where they replicate

Lymphocytes + fibroblasts surround the macrophage forming a defensive barrier (granuloma - AKA ghon focus) - pathogenesis of latent TB

^if this fails the mycobacterium can spread + cause extra-pulmonary TB

active infection: when malnourished, immunosuppressed or elderly, Ghon focus becomes reactivated → spreads to upper lobes (apex) of lungs (high oxygen area) → memory T-cells release massive amounts of cytokines → caseous necrosis causing cavitation → TB disseminates via pulmonary venous system → systemic Miliary TB

Miliary TB: whole body-wide haematogenous spread of TB, poor prognosis

71
Q

ACTIVE TUBERCULOSIS CLINICAL PRESENTATION

  • systemic? 5
  • pulmonary? 3
  • genitourinary? 3
  • MSK? 4
  • CNS? 1
  • Skin? 2
  • Pericardial? 3
  • GI? 2
  • adrenal? 1
A

SYSTEMIC

  • weight loss
  • fever
  • night sweats (+/-rigors)
  • anorexia
  • malaise
  • palpable LYMPH NODES (rubbery)

PULMONARY (70%)

  • persistent/chronic PRODUCTIVE COUGH (>3 wks)
  • breathlessness (late)
  • haemoptysis (late)

GENITO-URINARY

  • Sterile Pyuria (on MSU) or Haematuria
  • Dysuria or loin pain
  • Infertility (females) or Swollen epididymis (males) (or prostatitis symps)

MSK

  • joint pain (arthritis)
  • bone pain (osteomyelititis)
  • Pott’s disease (osteomyelitis + arthritis involving multiple vertebrae)
  • abscess formation (loin or psoas)

CNS
- TB meningitis (?presents same as normal meningitis? - think over 1-3wks though?)

SKIN

  • erythema nodosum
  • lupus vulgaris (painful nodular lesions affecting the face)

PERICARDIAL

  • SOB
  • chest pain
  • ankle swelling

GI

  • abdo pain / distension
  • constipation / bowel obstruction

ADRENAL
- presents as adrenal insufficiency

in children:

  • porr weight gain / faltering growth
  • fatigue
  • persistent fever

MILIARY = massive lymphohematogenous spread of Mycobacterium tuberculosis bacilli from a pulmonary or extrapulmonary focus with multiple organ involvement and very small granuloma lesions (1–2 mm)

72
Q

TUBERCULOSIS SCREENING:

  • who should be screened for TB? 7
  • 1st line screening test? 1 (what may cause a false negative test? 5)
  • 2nd line screening test? 1 (when is this used? 2)

describe findings of all of these

A

can’t find an exhaustive list but:

  • contacts of known positve cases
  • prisons
  • homeless people
  • new entrants from high prevelence country
  • immunocompromised (incl HIV)
  • about to start immunosuppression (eg anti- TNF drugs: infliximab - also need CXR)
  • new NHS employees

1) MANTOUX TEST
- tests for hypersensitivity to tuberculin
= positive if >5mm after 2-3 days (if <5mm can give BCG vaccine)
- if 6-15mm norm prev infection or BCG vaccine (don’t need BCG vaccine)
- if over 15mm highly suggestive of active TB disease

false negative mantoux test may be caused by:

  • miliary TB
  • HIV
  • sarcoidosis
  • lymphoma
  • very young age (eg <6 months)

2) INTERFERON GAMMA RELEASE ASSAY (IGRA) TEST
- blood test detecting response of WBCs to TB antigens

use if:

  • mantoux is positive or equivocal
  • mantoux test may be falsely negative (see above)

nb sometimes if someone high risk - just use IGRA first, instead of doing mantoux first!

nb the heaf test is NOT used anymore!

73
Q

TUIBERCULOSIS INVESTIGATIONS

  • gold standard diagnostic test? 1 (incl what stain is used?)
  • additional diagnostic test which gives faster results? 1
  • imaging to do in all? (classic findings? 2)

also describe findings of all of these

A

gold standard = SPUTUM CULTURE

  • 3 deep cough samples (one early morn)
  • stained with ZIEHL-NEELSON stain for acid-fast bacilli (all mycobacteria will stain positive!)
  • can take 1-3 weeks to come back
  • can also assess drug sensitivities!

nb can just do the stain and this is faster but less good! - called a sputum smear!

other = NUCLEIC ACID AMPLIFICATION TESTS (NAAT)

  • allows rapid diagnosis (within 24-48hrs)
  • more sensitive than smear but less sensitiove than culture
  • can show some drug resistance (but not as good as culture)

do CHEST X-RAY in ALL (ie ANY suspision of TB!)

  • upper lobe caviation
  • bilateral hilar lymphadenopathy

If think have EXTRA-PULMONARY TB - get a sample from this site / nearby lymph nodes if possible + try to culture

If have high suspision of TB - take cultures and then treat before they’ve come back!

74
Q

CXR findings in TB:

  • latent infection? 1
  • secondary / latent infection
A

LATENT
= Hilar lymphadenopathy, Ghon focus

SECONDARY / ACTIVE

  • Evidence of Apical consolidation
  • Cavitating lesions
  • Fibro-calcification → Tracheal shift toward Miliary lesion
    Reticular pattern (millet seeds)
  • multiple 1-9mm lesions across whole lung field

nb google x-ray for milliary TB

75
Q

management of TUBERCULOSIS:

  • antibiotics for ACTIVE? 4 (how long for each?)
  • antibiotics for LATENT? 2 (how long for?)
  • management of TB meningitis? 2
  • what additional intervention can sometimes be used to aid compliance?
  • additional thing to do if diagnose TB? 1
A

DO NOT DELAY TREATMENT IF WAITING FOR CXR/SPECIMEN RESULTS
Put patient in side room, limit contacts, treat symptoms

managed by specialist TB physician!

ACTIVE = "RIPE"
- Rifampicin (6 months)
- Isoniazid (6 months)
- Pyrazinamide (2 months)
- Ethambutol (2 months)
^all are 3 doses/wk

LATENT
- Rifampacin + Isoniazid for 3 months or Isoniazid alone for 6 months

TB MENINGITIS

  • same abx as for active (but continue R + I for 1 year, instead of 6 months!)
  • also have dexamethasone!

nb isoniazid is always with pyroxidine too!

if pts likely to have poor concordance (homeless, prison) then can do DIRECTLY OBSERVED therapy with 3x a week dosing!

TB = NOTIFIABLE DISEASE
- inform public health and do contact tracing!

76
Q

TB ANTIBIOTICS SIDE EFFECTS:

  • Rifampicin? 4
  • Isoniazid? 4
  • Pyrazinamide? 3 (+ 2 CIs)
  • Ethambutol? 1

incl which is PY450 inducer + inhibitor

A
RIFAMPICIN
= PY450 inducer
- flu-like symptoms
- hepatitis (?stop if LFT derange)
- orange secretions
ISONIAZID
= PY450 inhibitor
- peripheral neuropathy (prevent w pyroxidine = vit B6)
- hepatitis
- agranulocytosis
PYRAZINAMIDE
- hyperuricaemia -> gout
- arthralgia, myalgia
- hepatitis
CI: acute gout, porphyria

ETHAMBUTOL
- optic neuritis (check visual acuity before + during treatment)
^”eyes go blurry when you have ethanol!”

77
Q

Differential diagnoses for GRANULOMATOUS DISEASE

for each list:

  • risk factors
  • brief clinical presentation
  • biopsy findings
  • other lab findings
  • sarcoidosis
  • TB
  • hodgkin lymphoma
  • non-hodgkin lymphoma
  • pneumoconiosis
  • granulomatis w polyangitis (wegner’s)
  • histoplasmosis
A
SARCOIDOSIS
- RF: black women
- dry cough, erythema nodosum, lupus pernio, uveitis
= non-caseating granulomas, giant cells
- high ACE levels in blood

TUBERCULOSIS
- RF: immunocompromised, prev TB or recent TB exposure
- fever, weight loss, night sweats, productive cough (not responsive to pneumonia abx), haemoptysis
= caseating granuloma, langerhan giant cells, epithelioid macrophages, acid-fast bacilli

HODGKIN LYMPHOMA
- RF: EBV infection
- pel-ebstein fever, alvohol-induced pain, pruritis
= non-caseating granulomas, reed-sternberg cells, inflam cell infiltrates (eosinophils, fibroblasts, plasma cells)
- single or combined cytopenias (RBC, platelets, WBC)

NON-HODGKINS LYMPHOMA
- RF: infections (EBV, Hpylori), cell damage (toxins, immunosuppresion, radiation)
- lymph nodes, splenomegaly, evidence of bone marrow suppression
= non-caseating granulomas (NO reed-sternberg cells), B or T cells, inflamm cell infiltrate
- single or combined cytopenias

PNEUMOCONIOSIS
- RF: exposure to mineral dust (eg silica)
- often asymptomatic (may have: progressive exertional SOB, chronic cough, clubbing, crackles)
= non-caseating granulomas (silica/asbestos bodies)
- positive beryllium lymphocyte proliferation test (BeLPT)

GRANULOMATIS W POLYANGITIS (WEGNER'S)
- RF: white people 65-75years
- chronic rhinosinusitis with thick purulent/bloodty discharge, treatment resistant pneumonia, glomerulonephritis
= non-caseating granulomas
- positice c-ANCA

HISTOPLASMOSIS
- RF: HIV, exposure to bird/bat excrement
- pulmonary (dry cough, oral ulcers) or extra-pulm (splenomegaly)
= caseating granuloma, Identification of H. capsulatum yeast with silver stain
- Positive polysaccharide urine and serum antigen test

DON’T WORRY ABOUT THE RARER ONES AND DIAGNOSTIC TESTS TOO MUCH! - JUST BE AWARE OF DIFFERENT CAUSES OF GRANULOMATOUS DISEASES

78
Q

OBSTRUCTIVE SLEEP APNOEA:

  • describes what happens?
  • risk factors? (1 big, 3 causes of large tongue, 2 other)
A

intermittent closure/collapse of pharyngeal airway → apnoeic episodes during sleep → terminated by partial arousal

  • OBESITY

macroglossia:

  • acromegaly
  • hypothyroid
  • amyloidosis
  • marfans
  • large tonsils
79
Q

OBSTRUCTIVE SLEEP APNOEA

  • symptoms? 6
  • effect on physiology/complications? 3
A
  • Loud SNORING (often witnessed by parter, who may also witness partial apnoeas)
  • Daytime somnolence (falling asleep/fatigued in day)
  • Poor sleep quality
  • Morning headache
  • ↓ libido
  • ↓ cog performance

COMPLICATIONS

  • HTN
  • type 2 resp failure (resp acidosis w compensation)
  • pulmonary HTN
80
Q

OBSTRUCTIVE SLEEP APNOEA

  • screening / inital tests? 2
  • diagnostic test? 1
A
  • Epworth Sleepiness Scale (questionnaire completed by patient +/- partner)
  • Multiple Sleep Latency Test (MSLT) (measures the time to fall asleep in a dark room (using EEG criteria))

diagnostic = POLYSOMNOGRAPHY (sleep studies)

  • monitors O2 sats, airflow of now & mouth, ECG, EMG chest & abdo wall during sleep
  • numbewr of apnoeas determine if mild, mod or severe
81
Q

MANAGEMENT:

  • lifestyle? 3
  • 1st line if mod-severe? 1
  • other management options? 2
A
  • loose weight
  • decrease alcohol
  • decrease smoking

if mod/severe = air-driven CPAP overnight!

occasionally:

  • intra-oral devices
  • surgery to remove obstruction (eg tonsillectomy)
82
Q

CARBON MONOXIDE POISONING:

  • main risk factors? 3
  • main symptoms? 5
  • signs of severe toxicity? 5
A
  • fire/smoke inhalation
  • poor housing (eg student, caravans etc)
  • suicide attempt!
  • headache (90%)
  • nausea + vomiting (50%)
  • vertigo (50%)
  • confusion (30%)
  • subjective weakness (20%)

severe toxicity:

  • ‘pink’ skin and mucosae
  • hyperpyrexia
  • arrhythmias / ischaemias
  • extrapyramidal features
  • coma -> death
83
Q

CARBON MONOXIDE POISONING:

  • 1st line investigation if suspect? 1
  • additional bedside test to always do? 1
  • mainstay of management? 1 (be specific)
  • additional management? 2 (when are each of these indicated?)
A

O2 SATS ARE MISLEADING! (as they measure carboxy and oxyhaemoglobin!) - so will often have sats of 100%!

ABG ASAP (see conc of carboxyhaemoglobin - nb norm slightly raised in smokers!) - can use VBG if really struggling but levels not as reliable!

do ECG (look for arrythmias/ischaemia)

Mx: 100% OXYGEN NRBM

  • give for a min of 6hours
  • continue until all symptoms have resolved (ie rather than monitoring CO levels)

HYPERBARIC OXYGEN if:

  • any LOC
  • neuro signs (other than headache)
  • myocardial ischaemia or arrythmia
  • pregnancy

EARLY INTUBATION if:

  • poisoning as result of fire / inhalational injury
  • eg: Burns to the face Soot in nostrils or mouth and/or Stridor or hoarseness or drooling
84
Q

COAL WORKER’S PNEUMOCONIOSIS

  • meaning of pneumoconiosis?
  • clinical presentation?
A

Pneumoconiosis = accumulation of dust in the lungs and the response of the bodily tissue to its presence, most commonly used in relation to coal worker’s pneumoconiosis

often asymptomatic initially
- decades between exposure and symptoms

  • SOB on exertion
  • cough +/- black sputum

can present with really severe disease and generalised fibrosis!

85
Q

COAL WORKER’S PNEUMOCONIOSIS

  • finding on CXR?
  • finding on spirometry?
  • management?
A

CXR

  • UPPER LOBE FIBROSIS
  • Round irregular, nodular opacities in upper zones!!
  • can have bilateral hilar lymphadenopathy
  • can have mass like area of opacification (sausage shaped) in progressive massive fibrosis

SPIROMETRY

  • Obstructive: FEV1/FVC < 0.7, ↓↓FEV1 = Simple
  • Mixed obstructive/restrictive = Fibrosis

management is supportive! - incl chest physio etc

86
Q

ASBESTOS-RELATED CONDITIONS

difference between:

  • pleural plaques
  • pleural thickening
  • asbestosis
  • mesothelioma

in terms of:

  • CXR changes
  • clinical presentation
A

PLEURAL PLAQUES

  • benign, don’t become malignant (very clear on xray!)
  • most common form of asbestosis-related lung disease
  • latent period of 20-40 years

PLEURAL THICKENING
- looks like an empyema or haemothorax on CXR

ASBESTOSIS

  • severity is linked to length of exposure
  • latent period: 15-30 years
  • LOWER LOBE FIBROSIS
  • SOB + reduced exercise tolerance!

MESOTHELIOMA

  • Crocidolite (blue) asbestos is the most dangerous form
  • risk is unrelated to duration of exposure
  • progressive SOB, chest pain, pleural effusion

remember asbestosis is also a risk factor for normal lung Ca too!

nb for mesothelioma: Patients are usually offered palliative chemotherapy and there is also a limited role for surgery and radiotherapy. Unfortunately the prognosis is very poor, with a median survival from diagnosis of 8-14 months.

87
Q

LUNG ABSCESS

  • risk factors? 4
  • symptoms? 5 (esp ones specific to lung abscess)
A

RISK FACTORS:

  • high risk for aspiration (eg post-stroke, reduced GCS)
  • brochial obstruction (lung Ca, FB aspiration, bronchial stenosis)
  • immunocompromised state
  • pneumonia

SYMPTOMS

  • Cough with production of FOUL-SMELLING sputum
  • haemoptysis
  • SWINGING fever
  • night sweats
  • anorexia / weight loss
88
Q

LUNG ABSCESS

  • specific findings on CXR/CT scan? (incl norm location of abscess)
  • management? (1st + 2nd line)
A

ALSO do: Gram stain, culture, and sensitivity of expectorated sputum!!!

CXR/CT: irregular rounded cavity with an AIR-FLUID LEVEL that is dependent on body position (most commonly in the RIGHT lung)

1st) antibiotics that cover ANAEROBES!
2nd) if abx fail: drainage or surgical resection!

89
Q

EMPYEMA

  • what is it?
  • when to suspect?
  • investigations to do? 2 (incl findings)
  • management? 1
A

pus in pleural space

Suspect if pt w/ RESOLVING pneumonia develops FEVER

CXR
- pleural effusion (almost always unilateral!)

PLEURAL ASPIRATION

  • plurulent/ turbid/ yellow
  • low glucose
  • high LDH
  • pH < 7.2

treat with: CHEST DRAIN! (do repeat CXR before emove)

nb not ever pleural effusion associated with pneumonia is an empyema! - have to do aspiration to confirm!

90
Q

CAUSES of HAEMOPTYSIS:

  • causes due to severe lung inflammation? 3
  • pulmonary vascular disorders? 2
  • airway trauma? 3
  • others? 2

investigation for all? 1

A

SEVERE LUNG INFLAM

  • bronchiectasis
  • tuberculosis
  • aspergilloma

PULM VASCULAR

  • pulmonary embolism
  • raised pulm capillary pressure (ie pulm oedema secondary to LHF)

AIRWAY TRAUMA

  • incessant coughing
  • foreign body
  • iatrogenic

OTHERS

  • bronchogenic carcinoma
  • coagulopathy

nb also make sure it’s not coming from throat/nose or GI system!

do CXR whenever have haemoptysis! - if massive, stabilise before imaging!

91
Q

CYANOSIS

  • what is it? what is it a sign of?
  • where can you see it centrally?
  • where can you see it peripherally?
  • who is it a poor sign in?
A

skin appears dusky blue

sign of deoxygenation

central
- lips and tongue

peripheral
- limbs

poor sign in people who are not white!

92
Q

DEMENTIA

  • commonest causes? 3
  • other relatively common? 2
  • rarer causes? 5
A

= alzheimers (>50%)
= vascular dementia
= mixed alzheimers + vascular

  • frontotemporal dementia
  • lewy body dementia

RARE:

  • parkinsons dementia
  • huntington disease
  • CJD
  • HIV (50% of advanced HIV pts)
  • progressive supranuclear palsy (PSP)
93
Q

DIFFERENTIALS FOR DEMENTIA

  • endocrine? 2
  • vitamin deficienies? 3
  • infection? 1
  • stuff in brain? 3
  • psych? 2

(ie not different types of dementia, but things that can mimic them, and may be reversible)

A
  • hypothyroidism
  • addison’s
  • B12 deficiency
  • folate deficiency (B9)
  • thiamine deficiency (B1)
  • syphillis
  • normal pressure hydrocephalus
  • brain tumour
  • subdural haematoma
  • depression
  • chronic drug use (eg alcohol, barbituates)
94
Q

FRONTOTEMPORAL DEMENTIA:

  • aka?
  • briefly describe pathophysiology?
  • age normally starts in?
  • initial symptoms/signs?
  • later symptoms/signs?
A

aka PICK’S DISEASE
- nb technically pick’s disease is a sub-type of frontotemporal that can only be diagnosed on biopsy….

progressive degeneration of frontal and/or temporal lobe due to aggrigation of TAU PROTEIN to form PICKS BODIES

nb 10-20% are familial

onset = 40-60years

1st) INAPPROPRIATE SOCIAL BEHAVIOUR
- apathy
- disinhibition
- exagerated emotional displays
- irritability

LATER

  • aphasia
  • lack of attention
  • parkinsonism
  • pyramidal signs (eg hyperreflexia, babinski sign)

MEMORY GENERALLY REMAINS INTACT until very end!

nb alzheimers is still the most common type of dementia in this age group but this start with memory signs!

95
Q

FRONTOTEMPORAL DEMENTIA

  • aka?
  • what may see on imaging?
  • management?
  • prognosis?
A

aka PICK’S DISEASE
- nb technically pick’s disease is a sub-type of frontotemporal that can only be diagnosed on biopsy….

is a clinical diagnosis but may be:
- atrophy of frontal and/or temporal lobes on CT/MRI

general mx

  • supportive therapy (behavioural or speech)
  • exercise

meds

  • DON’T use cholinesterase inhibitors or memantadine (will make worse!)
  • may use meds for associated symptoms!

depression: SSRIs

agitation, hallucinations, insomnia: atypical antipsychotics (SGA)

prognosis is average 6 years from symptom onset

  • progression is faster than alzheimers
  • common cause of death is intercurrent infection, eg pneumonia!
96
Q

Creutzfeldt-Jakob disease

  • what % sporadic, familial and acquired?
  • pathophysiology?
  • two main characteristic features?
  • other clinical features?
A
  • sporadic (85%)
  • familial (10-15%)
  • acquired (<1%)

nb aquired can can be iatrogenic (via organ transplant or blood donation) or variant CJD (from injestion of beef infected with BSE)

CJD is caused by misfolded proteins (PRIONS, PrPSc) that are either produced by affected individual themselves, or taken up from an exogenous source

main features:
= RAPDILY progressive DEMENTIA (wks-months)
= MYOCLONIC JERKS

other features

  • cerebellar disturbances (eg gait instability) + extra-pyramidal deficits
  • seizures
  • akinetic mutism
  • visual hallucinations
  • depression

nb there other forms of prion diseases but CJD is by far the most common

97
Q

Creutzfeldt-Jakob disease

  • latency period?
  • investigations? (+findings)
  • finding on biopsy?
  • prognosis?
A

the latency period until symptom onset varies greatly with the type of exposition (e.g., between 5 and 30 years in some cases of iatrogenic CJD)

  • CSF (tau + other proteins)
  • MRI (Signal amplification in basal ganglia + head of the caudate nucleus
  • EEG (triphasic periodic sharp wave complexes with a frequency of 1–2 Hz)

nb don’t worry too much about findings - just know which investigations to do!

BIOPSY
= spongiform degeneration (e.g., intracytoplasmic vacuoles within the neurons of cerebral and cerebellar cortex that can be seen on H&E), gliosis (+ in rare cases, amyloid plaques)

sporadic CJD has life expectancy of 1 year from symptom onset (variant CJD is months)

main management is supportive + palliative care!

98
Q

AIDS-related dementia

  • briefly describe pathology?
  • what % of advanced HIV get it?
  • describe main features? 3
  • features in later stages? 3
A

Dissemination of HIV into the CNS (particularly in advanced HIV infection and/or untreated patients)
- is generally a diagnosis of exclusion in advanced HIV

30-50% of people with advanced/untreated HIV get it

subcortical dementia
= memory loss
= depression
= moevemtn disorders

progresses to severe neuro deficits:

  • impaired vigilance/concentraition
  • aphasia
  • gait disturbances
99
Q

AIDS-related dementia

  • finding on MRI?
  • finding on biopsy?
  • management? 2
A

MRI: multiple subcortical hyperintense non-enhancing lesions

BIOPSY
= giant cells with multiple nuclei (formed through fusion of HIV-infected monocytes)

Mx

  • HAART
  • supportive therapy (as with all dementias)
100
Q

HIV-ASSOCIATED CNS LESIONS:

for each briefly describe:

  • pathophysiology?
  • clinical features?
  • findings on neuroimaging +/or further tests?
  • management?
  • cerebral toxoplasmosis
  • primary CNS lymphoma
  • cerebral abscess
  • progressive multifocal leukoencephalopathy (PML)
  • HIV-associated encephalopathy / dementia
A

CEREBRAL TOXOPLASMOSIS (50%)
- reactivation of a prior infection w Toxoplasmosis Gondii (most common neurological AIDS-defining condition)
= headache, fever, altered mental state, seizures
- contrast CT: MULTIPLE RING-ENHANCED lesions (mainly in basal ganglia) - thallium SPECT NEGATIVE
- CSF: lots of lymphocytes, elevated protein
= Mx: pyrimethamine + sulfadiazine

PRIMARY CNS LYMPHOMA (30%)
- extra-nodal non-hodgkins lymphoma, associated with EBV infection
= headache, focal neuro deficits, neuropsych symps (eg personality changes), seizures (<15%)
- contrast CT: SINGLE SOLID (homogenous) enhanced lesion, thallium SPECT POSITIVE
- CSF: EBV positive (also do biopsy of lesion)
= Mx: high dose methotrexate +/- whole brain irradiation (plus steroids, after biopsy confirmed!)

CEREBRAL ABSCESS
- abscess formation (lots of different causes)
= disseminated infection, fever, headache, symptoms of raised ICP, neuro deficits, seizures
- contrast CT: focal intraparenchymal lesion with a central hypodense (necrotic) area and peripheral ring enhancement
- do biopsy to confirm!
= Mx: antibiotics +/- surgical drainage

PROGRESSIVE MULTIFOCAL LEUKOENCEPHALOPATHY (PML)
- Demyelinating disease of the CNS caused by reactivation of the JC virus
= rapidly progressing focal neuro deficits (eg visual field, hemiparesis), cognitive impairment, impaired vigilance
- contrast CT: disseminated, non-enhancing white matter lesions without mass effect
- CSF: JC virus DNA on PCR
- Mx: supportive therapy

HIV-ASSOCIATED DEMENTIA
- Dissemination of HIV into the CNS (norm a diagnosis of exclusion)
= subcortical dementia proggressing to severe neuro deficits
- MRI: multiple subcortical hyperintense non-enhancing lesions
- histopathology: giant cells with multiple nuclei
- Mx: HAART + supportive therapy

DON’T NEED TO KNOW ALL THESE (HIV-dementia was only a minor condition) - but I just found it interesting!
- actually be aware of them as AIDS-defining conditions!