7) repro, resp, psych Flashcards

Question 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

Answer

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

Question 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

Answer

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

Question 3

Q

ACUTE BACTERIAL PROSTATITS

abx management? for how long?
possible complications? 3

Answer

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

Question 4

Q

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

breifly describe how they present + mx

Answer

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)

Question 5

Q

BALANITIS:

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

Answer

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

Question 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

Answer

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

Question 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!

Answer

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

Question 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)

Answer

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

Question 9

Q

BALANITIS

complications? 4
possible mx of these?

Answer

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!)

Question 10

Q

PHIMOSIS

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

Answer

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)

Question 11

Q

PHIMOSIS

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

Answer

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)

Question 12

Q

PARAPHIMOSIS

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

Answer

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!!!

Question 13

Q

PARAPHIMOSIS

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

Answer

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!

Question 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

Answer

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!

Question 15

Q

Medications that can cause erectile dysfunction? 2

Answer

A

beta blockers

- SSRIs

Question 16

Q

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

Answer

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

Question 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

Answer

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

Question 18

Q

EPIDIDYMO-ORCHITIS

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

Answer

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

Question 19

Q

EPIDIDYMO-ORCHITIS:

- describe clinical presentation? (incl signs + symptoms)

Answer

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)

Question 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

Answer

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)

Question 21

Q

EPIDIDYMO-ORCHITIS:

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

Answer

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

Question 22

Q

EPIDIDYMO-ORCHITIS:

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

Answer

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!)

Question 23

Q

TESTICULAR CANCER

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

Answer

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!

Question 24

Q

TESTICULAR CANCER

most common presenting symptom? 1
other possible symptoms? 3

Answer

A

painless lump in testicles

pain (sometimes)
hydrocele
gynaecomastia

Question 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?

Answer

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

Question 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

Answer

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!

Question 27

Q

BREAST FIBROADENOMA

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

Answer

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

Question 28

Q

MASTITIS

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

Answer

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

Question 29

Q

MASTITIS

local symptoms? 3
possible systemic symptoms? 3

Answer

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

Question 30

Q

MASTITIS

1st line management? 1
symptomatic relief? 2
indications for Abx? 3 (which abx?)
possible complciation? 1

Answer

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

Question 31

Q

BREAST ABSCESS

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

Answer

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

Question 32

Q

FAT NECROSIS OF BREAST

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

Answer

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!

Question 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

Answer

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.

Question 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?

Answer

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

Question 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

Answer

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)

Question 36

Q

NIPPLE DISCHARGE

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

Answer

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

Question 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

Answer

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)

Question 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

Answer

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

Question 39

Q

BREAST LUMP REFERRAL:

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

Answer

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

Question 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

Answer

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

Question 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

Answer

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!

Question 42

Q

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

Answer

A

USS scrotum

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

DON’T biopsy trough scrotum!!

Question 43

Q

Mx of some testicular masses:

torsion of testicular appendage
hydrocele
spermatocele
varicocele
scrotal hernia

Answer

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

Question 44

Q

HYPERVENTILATION / PANIC ATTACK

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

Answer

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

Question 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

Answer

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

Question 46

Q

ACUTE BRONCHITIS:

describe pathophysiology?
normal causative organism?

Answer

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

Question 47

Q

ACUTE BRONCHITIS

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

Answer

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!)

Question 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

Answer

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

Question 49

Q

DDx of ACUTE COUGH

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

Answer

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?

Question 50

Q

SPONTANEOUS PNEUMOTHORAX

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

Answer

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 #)

Question 51

Q

RED FLAGS for TENSION PNEUMOTHORAX? 8

Answer

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

Question 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)

Answer

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!

Question 53

Q

Management of PRIMARY SPONTANEOUS PNEUMOTHORAX:

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

Additional advice for all? 1

Answer

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)

Question 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

Answer

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

Question 55

Q

Management options if recurrent pneumothoraces? 2

Answer

A

1) Surgery to remove bullae / diseased lung

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

Question 56

Q

PLEURAL EFFUSION

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

Answer

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

Question 57

Q

CAUSES of PLEURAL EFFUSIONS:

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

Answer

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

Question 58

Q

PLEURAL EFFUSION:

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

Answer

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

Question 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?

Answer

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)

Question 60

Q

PLEURAL EFFUSION

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

Answer

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!

Question 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!

Answer

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

Question 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?

Answer

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

Question 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?

Answer

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!!

Question 64

Q

SARCOIDOSIS

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

Answer

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!)

Answer 65

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

Answer 66

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

Answer 67

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

Answer 68

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!

Answer 69

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)

Answer 70

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

Answer 71

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)

Answer 72

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!

Answer 73

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!

Answer 74

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

Answer 75

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!

Answer 76

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!”

Answer 77

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

Answer 78

A

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

OBESITY

macroglossia:

acromegaly
hypothyroid
amyloidosis
marfans
large tonsils

Answer 79

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

Answer 80

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

Answer 81

A

loose weight
decrease alcohol
decrease smoking

if mod/severe = air-driven CPAP overnight!

occasionally:

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

Answer 82

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

Answer 83

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

Answer 84

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!

Answer 85

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

Answer 86

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.

Answer 87

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

Answer 88

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!

Answer 89

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!

Answer 90

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!

Answer 91

A

skin appears dusky blue

sign of deoxygenation

central
- lips and tongue

peripheral
- limbs

poor sign in people who are not white!

Answer 92

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)

Answer 93

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)

Answer 94

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!

Answer 95

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!

Answer 96

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

Answer 97

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!

Answer 98

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

Answer 99

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)

Answer 100

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!

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7) repro, resp, psych Flashcards

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