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EXAM 2 > Rapid R/V (400) > Flashcards

Rapid R/V (400) Flashcards

1
Q

What happens when a cervical rib becomes symptomatic?

A
  • rarely it may cause pressure on the SUBCLAVIAN vessels & brachial plexus -> transient vascular insufficiency or paraesthesian in the UL
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2
Q

diarrhoea, weight loss, abdominal discomfit + selective IgA deficiency - Dx?

A

COELIAC disease

  • anti-endoyosial Ab are IgA Ab therefore will not be detected in people with low IgA Ab levels
  • i.e. need to be aware of serum IgA levels before interpreting anti-endomyosial Ab in pts with malabsorption
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3
Q

asthma + eosinophilia + rapidly progressive glomerulonephritis - Dx?

A
  • Churg-Strauss syndrome
  • poor prognosis with 25% 5year survival rate, can be increased with steroid Rx, if acute vasculitis then combo therapy with cyclophosphamide
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4
Q

Features of Churg-Strauss syndrome?

A
  • small vessel vasculitis
  • cutaneous vasculitic lesions
  • eosinophilia (<2)
  • asthma (mild)
  • mononeuritis/polyneuropathy
  • rarely 10% have glomerulonephritis
  • can have GI & cardiac involvement as well
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5
Q

Clinical presentation of Churg-strauss syndrome?

A
  • Pulmonary predominate: paroxysmal asthma attacks, fleeting pulmonary infiltrates - asthma may be present for years before overt features of multi-system vasculitis
  • skin lesions in 70%: e.g. purpura, cutaneous & subcut nodules
  • GI complications inc mesenteric ischaemia or GI haemorrhage
  • cardiac involvement is usually myo-pericarditis
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6
Q

4 causes of renal failure + eosinophilia? RACC

A
  1. Rapidly progressive glomerulonephritis
  2. Acute tubule-interstitial nephritis
  3. Churg-Strauss syndrome
  4. Cholesterol micro-emboli
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7
Q

How to Dx Churg-Strauss syndrome?

- ACR 1990 criteria?

A
  • clinical Dx supported by necrotising granulomatous vasculitis with extravascular eosinophilic infiltration on lung, renal or sural biopsy
  • serum pANCA (MPO) also elevated but also is in microscopic polyangitis
    4 out of the following:
  • asthma
  • eosinophilia (10% WCC differential)
  • mononeuropathy/polyneuropathy
  • migratory/transient pulmonary infiltrates
  • systemic vasculitis (cardiac, renal, hepatic)
  • extravascular eosinophils on a Bx inc artery, arteriole or venule
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8
Q

insulin-dependent diabetes with abnormal LFTs and low testosterone with inappropriately low gonadotrophin response
- what’s the Dx? test to confirm?

A

HAEMOCHROMATOSIS

  • pancreatic involvement, hepatic infiltration, iron deposition in pituitary
  • FERRITIN level - >500 is Dx
  • Nb in the absence of iron overload, chronic viral hepatitis, NASH, PCT, eton-related liver disease can also cause liver disease with increased serum ferritin (acute phase protein)
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9
Q

commonest endocrine deficiency in hereditary haemochromatosis?

A

= 2ry hypogonadism (iron deposition in pituitary) e.g. leading to impotence

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10
Q

Complications of iron overload in haemochromatosis?

A
  • increased risk of HCC
  • increased risk of hypothyroidism
  • susceptible to siderophoric (iron-loving) organisms e.g. Listeria spp, Yersinia enterocolitica & Vibrio vulnificus (uncooked seafood)
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11
Q

RFs for severe hepatic injury after paracetamol OD?

King’s college criteria for for liver Tx?

A

PT>20seconds 24h after ingestion
pH <7.3
Cr>300

  1. pH <7.3 24h after ingestion or
  2. PT>100s, Cr>300, grade III/IV encephalopathy
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12
Q

Diarrhoea + biochemical evidence of cholestasis i.e. ALP>transaminase - Dx?

A

PSC: primary sclerosing cholangitis
- raised ALP in a pt with UC in the absence of bone disease should raise suspicion of PSC - frequency of PSC is inversely proportional to severity of UC

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13
Q

Main pathological feature of PSC?

Presentation?

A
  • immunological destruction of intra & extra-hepatic bile ducts
  • 90% PSC ass with IBD, esp UC
  • UC is most frequent association with PSC
  • can be aSx but present with advanced liver disease
  • fatigue & pruritus common complaints (like other cholestatic disorders)
  • 1/5th complain of RUQ pain
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14
Q

How to Dx PSC?
Complications?
Rx?

A
  • ERCP: strictures within biliary ducts
  • i.e. complications of chronic cholestasis: steatorrhoea, fat-soluble vitamin malabsorption, large biliary strictures, cholangitis, cholangiocarcinoma, colonic carcinoma
  • Rx with cholestyramine to reduce pruritus; fat-soluble vitamin supplementation
  • must have Abx prophylaxis during instrumentation of biliary tree to reduce risk of bacterial cholangitis e.g. Ciprofloxacin
  • biliary stunting may improve biochemistry & Sx but definitive Rx = liver Tx!!!
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15
Q

LFT picture in Wilson’s disease?

A
  • hepatitic*
  • abnormal copper metabolism
  • neuro-psychiatric disease
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16
Q

Cyclophosphamide - MoA?

Adverse effects?

A
  • alkylating agent that causes cross-linking of DNA
  • haemorrhagic cystitis (incidence reduced with use of hydration & meson)
  • myelosuppression
  • TCC
  • rarely can cause lung fibrosis with concomitant pulmonary radiation Rx, or when having taken other drugs ass with pulmonary toxicity - e.g. after taking low doses for long periods
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17
Q

When can cyclophosphamide cause lung fibrosis?
- cyclophosphamide is metabolised in the liver to toxic metabolites which are responsible for lung damage
Dx?

A
  • rarely can cause lung fibrosis with concomitant pulmonary radiation Rx, or when having taken other drugs ass with pulmonary toxicity - e.g. after taking low doses for long periods
  • presents several years after cessation of the drug and deterioration of Sx with time
  • progresses and inevitably results in terminal respiratory failure
  • minimally responsive to steroids
  • does not usually cause clubbing & fine end-inspiratory crackles

Dx: clinical, CXR - reticulo-nodular shadowing of the upper zones, PFTs: restrictive lung defect; lung Bx not helpful

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18
Q

Causes of drug-induced lung fibrosis?

A
  • methotrexate
  • amiodarone
  • nitrofurantoin
  • ethambutol
  • cyclophosphamide
  • penicillamine
  • bleomycin
  • busulphan, methysergide, minocycline
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19
Q

Acute lung damage with cyclophosphamide Rx?

A
  • acute pneumonitis can occur with cough, dyspnoea, hypoxia & BL nodular opacities in the upper zones
  • responds to cessation of the drug & steroid therapy
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20
Q

Radiation-induced fibrosis - how does it present? clinical picture?

A
  • pneumonitis with cough, dyspnoea, restrictive lung defect, low transfer factor
  • more common when also taking e.g. bleomycin, cyclophosphamide
  • many pts show improvement & Sx AND PFTs within 18months of stopping radiotherapy (i.e. not associated with inexorable decline)
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21
Q

Head injury leading to low sodium, possibility of 2ry hypothyroidism, v high cortisol - Dx?

A

SIADH
sick euthyroid (or genuine acquired central transient hypothyroidism - may be protective in severe illness by preventing XS tissue catabolism) - repeat TFTs at least 6wks after recovery
v high cortisol indicates pituitary is working (i.e. stress response)

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22
Q

When to prescribe Ramipril/ACE-I in vascular disease?

A

Everyone with IHD/CAD/CVD/PVD/DM + 1 other RF for coronary artery disease

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23
Q

Criteria for Dx of polycythaemia rubra vera?

Sx of PRV?

A 
Raised red cell mass &amp; normal pO2 with either:
- splenomegaly 
- or 2 of the following:
WCC>12
Plts>400
raised B12 binding protein
low neutrophil ALP concentration
  • headaches & lethargy are common, due to hyper viscosity & raised IL-6 levels
  • visual disturbance, abdominal pain, pruritus
  • Nb palpable spleen is absent in 1/3rd
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24
Q

systolic murmur + right ventricular hypertrophy on ECG - Dx?

A

pulmonary stenosis

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25
Q

what is cryoglobulinaemia?

A

Its which undergo reversible precipitation at 4degC, dissolve when warmed to 37C
- 1/3 cases idiopathic

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26
Q

Type I cryoglobulinaemia 25%

  • type of Ig?
  • ass conditions?
A
  • monoclonal IgG/M

- multiple myeloma & Waldenstrom’s macroglobulinaemia

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27
Q

Type II cryoglobulinaemia 25%

  • type of Ig?
  • ass conditions?
A
  • mixed monoclonal (RF IgM) & polyclonal IgG

- hep C, hep B, RA, Sjogren’s, lymphoma

28
Q

type III cryoglobulinaemia 50%

  • type of Ig?
  • ass conditions?
A
  • polyclonal Ig (RF) or mixed IgG

- RA, Sjogren’s, chronic inflammation, hep B, lymphoproliferative dusease

29
Q

Sx of cryoglobulinaemia if present in high concentrations?
tests?
Rx?

A
  • Raynaud’s (only type I)
  • cutaneous: vascular purpura, distal ulceration
  • arthralgia
  • renal involvement: diffuse GN
  • hepatosplenomegaly
  • low complement (esp C4), high ESR
  • skin Bx if purpura
  • HCV thought to play an aetiological role in development of type 2 & 3 therefore Ix should always inc hep C serology
  • Rx with immunosuppression
  • plasmapheresis if severe renal impairment or acronecrosis
  • otherwise prednisolone & cyclophosphamide or chlorambucil
  • if 2ry to HCV then treat HCV e.g. peg IFN-alpha & Ribavarin (caution in renal failure)
30
Q

MoA of penicillamine? Adverse effects?

A
  • largely unknown but thought to reduce IL-1 synthesis & prevent maturation of newly synthesised collagen
  • rash, taste disturbance, proteinuria
31
Q

Causes of heavy proteinuria 2ry to membranous nephropathy in RA?

A
  • gold
  • penicillamine - occurs within 6-12months of initiation and proteinuria resolves after stopping (but may take several months)
32
Q

Causes of renal disease in RA?

A
  • drug-induced membranous nephropathy leading to proteinuria (gold, penicillamine)
  • renal amyloid ( proteinuria)
  • analgesic nephropathy (haematuria)
  • focal segmental glomerulonephritis (red cells in urine)
  • rheumatoid vasculitis (but usually affects skin & peripheral neuropathy; more likely in pts with severe disease, nodule formation, high titres of RF & low complement)
33
Q

MRI scans: what info does T1 weighted imaging provide?
what is low signal (black)?
what is intermediate signal (grey)?
what is high signal (white)?

A
  • T1 = ANATOMICAL
  • black = bone, air, CSF, rapidly flowing blood
  • grey = grey matter is darker than white
  • white = fat in bone, scalp & orbit
34
Q

MRI scans: what info does T2 weighted imaging provide?

A
  • T2 = PATHOLOGICAL
  • black = bone, air, rapidly flowing blood, haemosiderin
  • grey = WHITE matter is darker than grey matter
  • white = CSF/water
35
Q

What Abx inhibit (& therefore precipitate toxicity of) aminophylline metabolism?
Features of theophylline toxicity?

A
  • Quinolones & Macrolides
  • also cimetidine, propranolol allopurinol, thiobendazole, the pill
  • nausea, vomit, hypotension, arrhythmia, hypokalaemia, acidosis, seizures
  • Sx occur when plasma theo conc >20mg/l, adverse at >40
36
Q

Rx of theophylline toxicity?

A
  • supportive
  • consider gastric lavage if <1hr since ingestion
  • activated charcoal
  • whole-bowel irrigation can work if theophylline is sustained release form
  • charcoal haemoperfusion is preferable to HD

Strategy 1 if pt stable:
- gastric lavage then oral activated charcoal

Strategy 2:

  • can treat arrhythmias with beta-blocker if not C/I, otherwise can use lignocaine for ventricular arrythmias & verapamil for supraventricular arrhythmias inc AF
  • treat seizures with diazepam/barbiturates (phenytoin not effective)

Strategy 3 (rarely required):

  • dialysis if level ?100 who have profound hypotension, fatal cardiac arrhythmias & seizures
  • age & hepatic disease are important factors to prognosis e.g. pts>60 with liver disease may be dialysed at levels >60
37
Q

6wk Hx of cough, sputum, eosinophilia & perihelia infiltrates - Dx?

A

ABPA: allergic bronchopulmonary aspergillosis

- e.g. asthma, proximal bronchiectasis, parenchymal infiltrates in perihilar area

38
Q

Confirm Dx & Rx for ABPA?

A
  • high IgE & IgG Ab
  • positive hypersensitivity skin test to Aspergillus fumigates
  • Rx with prolonged itraconazole
39
Q

What is tropical pulmonary eosinophilia?

A
  • immune reaction to infection with human filarial parasites Wucheria bancrofti & Brugia malayi
  • non-productive cough, wheeze, fever, weight loss, lymphadenopathy, eosinophilia & patchy infiltrates on CXR
  • occurs in pts infected in the tropics
  • worm rarely identified but it responds to diethycarbamazine (used to treat filariasis)
40
Q

Fluid of choice in HONK?

A
  1. 9% saline
    - effective at restoring volume and has lower risk of causing large drops in plasma osmolality (a RF for developing cerebral oedema)
    - if despite this, Na is >150, can consider 0.45% saline
    - Nb severe dehydration leads to hyper viscosity that can predispose to arterial & venous thromboses -> heparin needed
41
Q

What is Henoch-Schonlein purpura?

complications?

A
  • IgA mediated small vessel vasculitis in age 4-15
  • lower abdo pain, bloody diarrhoea, large joint arthralgia, purpuric rash & nephritis
  • intestinal perforation, haemorrhage, intussusception, acute renal failure
42
Q

How to Dx HSP?

A
  • clinical
  • skin Bx for tissue Dx - leucoclastic vasculitis with IgA deposition
  • renal Bx - mesangial IgA deposition ass with a glomerulonephritis (indistinguishable from IgA nephropathy)
  • serum IgA levels low in 50%
43
Q

Complications/manifestations of meningococcal meningitis & septicaemia?

A
  • caused by serogroups B & C
  • septicaemia ass with widespread petechial haemorrhage
  • conjunctival haemorrhage may be 1st physical manifestation
  • shock is common due to production of a circulating endotoxin
  • DIC can occur
  • which can result in adrenal haemorrhage (Waterhouse-Friderichsen syndrome)
  • can do blood cultures, and gram stain on CSF
  • focal neuro signs less common than with pneumococcal meningitis
44
Q

MoA of n-acetyl cysteine in paracetamol OD?

A
  • cont giving while LFTs abnormal
  • replenishes cellular glutathione stores & reduces oxidative damage caused by the toxic metabolite NAPQI
    (paracetamol produces toxic metabolite NAPQI which is usually immediately conjugated with glutathione & excreted - but in XS it depletes cellular glutathione, so NAPQI accumulates -> hepatic necrosis & failure)
45
Q

how to calculate plasma osmolality?

A

2(Na + K) + urea + glucose

Nb etoh increases plasma osmolality

46
Q

2 causes of a low urine osmolality?

A
  • nephrogenic diabetes insipidus (e.g. lithium Rx)

- inhibition of ADH secretion e.g. etoh ingestion

47
Q

Renal cell ca - where does it arise from? commonest histological subtype?
Associations?

A
  • proximal renal tubular epithelium
  • clear cell
  • more common in middle-aged men
  • smoking
  • von Hippel-Lindau syndrome
  • tuberous sclerosis
48
Q

Features of renal cell cancer?

A
  1. haematuria 2. loin pain 3. abdo mass
    - PUO
    - left varicocele (due to occlusion of left testicular vein)
    - 25% have mets at presentation
    - endocrine effects: EPO (polycythaemia), PTH (hypercalcaemia), renin (hypokalaemia, hypotension), ACTH
49
Q

Rx of renal cell cancer?

A
  • partial/total nephrectomy for confined disease
  • alpha-IFN & IL-2 have been used to reduce tumour size and treat pts with mets
  • receptor tyrosine kinase inhibitors e.g. sorafenib, sunitinib have been shown to have superior efficacy to IFN-alpha
50
Q

helpful Ix of RCC?

A

renal angiography & venography - allow assessment of invasion of veins & vascularity of the tumour
- bone scan to detect bony mets

51
Q

EPSEs of e.g. Haloperidol?

A
  • block dopamine in basal ganglia
  • tremor, dystonia, akathisia, parkinsonism, tardive dyskinesia
  • chronic tardive dyskinesias most common serious complications - affect 20% on chronic neuroleptics, occurring after been on Rx for at least 3months and can worsen in first few weeks after stopping - 60% resolve 3yrs after drug stopping - lip smacking, tongue protrusion, orofacial mouthing, trunk rocking, distal chorea
  • acute dystonic reactions occur within first few hours/days - oculogyric crisis, torticollis, truisms
  • uncommon, resolve as soon as drug stopped
52
Q

Causes of urogenital ulcers?

A
  • Behcets syndrome
  • Crohn’s, UC
  • herpes simplex virus
  • Reiter’s syndrome
  • lichen planus
  • syphilis
  • gonococcal
  • HIV
  • pemphigus pemphigoid
  • stevens-johnson syndrome
53
Q

what is Reiter’s syndrome?

A
  • classically conjunctivitis, urethritis, asymmetrical arthritis 1-4wks after bacterial dysentery or a sexually transmitted urethritis
  • other features: plantar fasciitis, achilles tendonitis, keratoderma blenorrhagica, circinate balanitis, stomatitis, hepatitis, cardiac/neuro involvement
  • venous thrombosis affects 4% and occurs early on
  • painless mouth ulcers
54
Q

causes of orogenital ulcers & venous thromboses?

A
  • Behcets syndrome
  • Crohns disease
  • UC
  • Reiter’s syndrome
55
Q

What is Behcet’s syndrome?

What are the clinical features?

A
  • recurrent multifocal disorder, persists over many years
  • recurrent mouth & genital ulcers, ocular lesions, skin, joint, neuro involvement
  • high incidence in mediterranean & japan
  • pharynx ulcers -> dysphagia, genital ulcers -> dysuria, dyspareunia
  • ocular most serious (rec uveitis, iridocyclitis, retinal vascular lesions, optic atrophy -> loss of vision in 50%)
  • skin: erythema nodosum, diffuse pustular rash affecting face, erythema multiforme
  • pricking skin leads to erythema within 24-48h
  • seronegative arthritis affects 40%: knees, ankles, wrists
  • rec thrombophlebitis of legs -> venous thrombosis, less often SVC/IVC thrombosis
  • neuro: confusion, meningoencephalitis, brainstem syndrome, MS, parkinsonian-type disorders
  • aSx proteinuria, abdo pain, diarrhoea can also occur
56
Q

How to Dx Behcet’s syndrome?

Rx?

A
  • clinical Dx
  • HLA-B51, B12, DR2, DR7 & Drw52 are ass
  • immune complexes present, elevated acute phase proteins
  • pathergy test of skin prick leading to erythema
  • topical steroids for genital ulcers & oral complicatins
  • systemic steroids if severe, & azathioprine as a steroid-sparing agent
  • colchicine, ciclosporin, levamisole can be used
57
Q

Causes of Roth spots? (haemorrhagic areas with a pale centre in the retina)

A
  • infective endocarditis
  • SLE
  • polyarteritis nodosa
  • severe anaemia
  • leukaemia
58
Q

Clinical features of endocarditis?

A
  • fever, murmur
  • splinter haemorrhages
  • osler nodes (small, painful)
  • janeway lesions (macular, painless)
  • roth spots
  • splenomegaly
  • microscopic haematuria/nephritis
59
Q

Causes of culture-negative endocarditis?

A

Non-infective (v rare): SLE (Libmann-Sacs), marantic endocarditis (malignancy)
Infective: brucella, coxiella burnetti, chlamydia, mycoplasma, legionella, histoplasmosis, tropherema whipelli, fungi (eg immunocompromised)

60
Q

Single best Ix for infective endocarditis?

A

TOE

  • blood cultures v useful and positive in 90% (e.g. prior Rx with Abx or a fastidious organism)
  • TTE doesn’t exclude IE as vegetations <3mm won’t show up
61
Q

Triad of cholangitis?
Commonest organism?
Ix?

A 
fever
RUQ pain
jaundice
- E. coli on blood cultures
- US liver to exclude a 2ry hepatic abscess, and to assess the CBD
- can do therapeutic ERCP/sphincterotomy
62
Q

How does cholangiocarcinoma usually present?

A
  • intermittent jaundice, causing duct obstruction before the onset of biliary cirrhosis
63
Q

Causes of combined respiratory & metabolic acidosis?

A
  • aspirin poisoning
  • acute renal failure & fluid overload
  • acute cardiac failure (pulmonary oedema -> hypoxia -> resp acidosis & renal hypo perfusion ->renal failure metabolic acidosis)
  • septicaemia from any cause complicated by ARDS
  • severe pneumonia with renal failure due to septicaemia or interstitial nephritis (Legionnaire’s disease)
  • malaria complicated by pneumonia
  • acute massive PE
  • cardiac arrest (before ventilation)
  • renal pulmonary syndromes: anti-GBM disease, Wegener’s granulomatosis, microscopic polyarteritis nodosa
64
Q

What is histiocytosis X?
clinical features?
Dx? Rx?

A
  • benign, unknown aetiology, multi-system but in 25% only 1 system affected
  • peak age presentation age 2-4yrs, affects M>F
  • skin, bones, ears, lungs, eyes, reticuloendothelial & CNS most often affected
  • skin rash common
  • individual histiocytomas are pinkish-brown papule 1-5mm diameter
  • resp: lung fibrosis, bullae & large airway obstruction by histiocytomas therefore both restrictive & obstructive defect can occur
  • bone: marrow infiltration may be ass with pancytopenia; usually skull - large radiolucent lesions
  • otitis externa, ear discharge
  • ocular: retro-orbital mass -> proptosis
  • hepatosplenomegaly, LN
  • 1/3rd develop diabetes INSIPIDUS due to histiocytic infiltration of pituitary stalk
  • SCC in exceptional cases
  • Dx: histiocytes & small round cells in histological specimens of affected tissues
  • Rx: steroids, in some cases cytotoxics, in some spontaneous regression
65
Q

Amiodarone MoA?
side-effects?
complications?

A
  • class III anti-arrhythmic effective in SVT & ventricular arrhythmias
  • SEs: nausea, metallic taste, tremor, nightmares, headaches, rashes inc photosensitive, slate-grey skin, corneal deposits
  • complications: optic neuritis, peripheral neuropathy, myopathy, hepatitis/cirrhosis, alveolitis, hyper/hypothyroidism, epididymitis, conduction taste disturbances

EXAM 2 (10 decks)

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