Revision Flashcards

1
Q

Definition pyrexia of unknown origin

A

Fever >38.3 multiple occasions

Fever > 3 weeks

One week of appropriate investigations in hospital

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2
Q

DDx pyrexia of unknown origin

A
Infection (BOATS)
-bacterial endocarditis (coxiella, HACEK)
-osteomyelitis
-abscess (abdominal/pelvic)
-TB
Connective tissue disease
-adult still
-giant cell
-PAD/takayasu/ANCA
Malignancy
-lymphoma
-leukemia
-RCC
-hepatocellular
Drugs (drug fever)
-antimicrobials
-antihistamines
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3
Q

History pyrexia of unknown origin

A

DETAILS

  • Drugs
  • Exposures (contacts, occupational)
  • Travel
  • Animals
  • Immunosuppression (HIV)
  • Localising symptoms
  • Sexual Hx
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4
Q

Investigations pyrexia of unknown origin

A

Urinalysis
Urine culture

3x Blood culture

FBC
-differentials
-film
EUC
LFT
ESR/CRP
PEP
ANA
RF
Mantou or IGRA
HIV serology
Heterophile antibody

CXR
Abdo ultrasound

Nuclear medicine (consider)

  • FDG PET CT
  • gallium-67 or indium-111–labeled leukocyte scintigraphy
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5
Q

Pathophys fever

A

Pyrogens

  • exogenous
  • > endotoxin (lipopolysaccharide on G neg bacteria)
  • > superantigens for staph aureus
  • endogenous cytokines
  • > IL-1
  • > IL-6
  • > TNF alpha
  • > can be induced or released by micro-organisms
  • > can be released in sterile inflammatory conditions (eg. pericarditis)

Elevation of hypothalamic set point

  • Endogenous/exogenous pyrogens enter systemic circulation
  • interact with endothelium of organum vasculosum of lamina terminalis
  • > network of englarged capillaries
  • > surrounds hypothalamus regulatory centers
  • Release of PGE2 on hypothalamus side of endothelium
  • Binding to EP-3 receptor on glial cells
  • > release of cAMP
  • Acts as neurotransmitter
  • > activates neuronal endings from thermoregulatory center
  • Elevation of set point
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6
Q

AKI ddx

A
PRE
Hypovolaemia
Decreased cardiac output
Decreased effective circulating volume
-CCF
-Cirrhosis 
Impaired autoregulation
-NSAIDs
-ARBs
-ACEI

INTRINSIC

Glomerular (Mindful Sailors Invest In A Good Anchor):

  • membranoproliferative
  • SLE
  • IgA
  • infectious (eg. post strep)
  • anti GBM
  • good pastures
  • ANCA (polyangitis with granulomatosis, microscopic polyangitis, eosinophilic granulomatosis with polyangitis)

Vascular (Some Honest Virgins Admit Masturbating Every Day They Can):

small:

  • Scleroderma
  • Hypertension (malignant)
  • Vasculitis
  • Atheroemboli
  • Microangiopathies

large:

  • Embolus (systemic/renal)
  • Dissection (aortic)
  • Thrombosis (renal vein)
  • Compartment syndrome (abdo)

Tubulointerstitial (Indoor Dogs Should SIT on their MAT)

interstitial nephritis:

  • Infections (legonella)
  • Drugs (antibiotics, NSAIDs)
  • Systemic (sarcoid, srjogens, SLE)

ATN:

  • Sepsis
  • Ischaemia
  • Toxins (vanc, aminoglycosides, contrast)

tubular obstruction:

  • Myeloma
  • Acyclovir
  • Tumor lysis syndrome

POST

Prostate
-BPH
-neoplasia
Bladder
-neurogenic
-anti-cholinergics
Urethra
intraluminal
-clots
-calculi
-necrotic papillae
intramural
-neoplasia
extramural
-neoplasia
-iatrogenic
-retroperitoneal fibrosis
-abscess
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7
Q

AKI investigations

A
VBG/ABG
-high anion gap = decreased GFR and retention of acids
-normal anion gap with high urine pH = renal tubular acidosis (Type 1 with impaired distal H secretion; Type 2 with impaired proximal bicarb reabsorption)
Urinalysis
Urine chemistries
-FENa (<1 = pre-renal, >2=ATN)
-FEUrea when diuretics (<35=pre-renal, >65=ATN)
Urine osmolality
-increased = pre-renal
-decreased = ATN
ECG
-hyperkalaemia
FBC
-anaemia (haemolysis, microangiopathies, myeloma)
-eosinophilia (interstitial nephritis, emboli, vasculitides)
-thrombocytopenia (microangiopathy)
EUC
-eGFR
-urea:creatinine ratio >20 = pre-renal
-hyperkalaemia
CMP
-hyperphosphataemia
-hypocalcaemia
Renal ultrasound/CT
-obstruction
-architecture 
Chest xray
-CCF
-Pulmonary oedema

Consider (in glomerulonephritis)

  • ANA/anti-DSDNA = lupus
  • C3/4 = immune complex GN types
  • anti-GBM antibodies
  • ANCAs
  • cryoglobin
  • anti-streptolysin O (post strep), hep (membranoproliferative) and HIV serology based on Hx
  • biopsy
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8
Q

ddx haematuria

A

NIICCKSS

neoplasm

  • kidney (RCC, transitional)
  • bladder (urothelial, squamous)
  • penile (squamous)
  • ureter
  • prostate (BPH/cancer)

Infection

  • UTI
  • pyelonephritis

Inflammation

  • prostatitis
  • cystitis
  • diverticulitis

Cysts
-PCKD

Coagulopathy

  • medical (eg. von willebrand, platlete (MAID FLUID), haemophilia, vessel wall)
  • drugs
Kidney injury (glomerular)
-Mindful Sailors Invest In A Good ANCA

Stones

  • renal
  • bladder

Staining

  • beets
  • phenazopyridine
  • rifampicin
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9
Q

anaphylaxis pathophys

A

Type 1 (IgE) mediated hypersensitivity

  • anaphylactoid
  • > direct activation of mast cells by agents eg. vanc
  • sensitisation
  • > exposure to allergen
  • > clonal expansion and class switching to IgE plasma/memory by cells
  • > driven by Th2 cells and interleukins
  • > IgE secreted systemically and constitutively occupies IgE high affinity receptor on mast cells (and basophils)
  • second exposure
  • > binding of allergen to IgE on mast cells causes receptor cross linking
  • mast cell activation and degranulation
  • > release of preformed mediators eg histamine and tryptase
  • > formation of eicosanoids eg cysteinyl LT’s and PGD2
  • > release of inflammatory cytokines eg TNF α

effect of mediators

  • histamine
  • > H1 and H2 receptors mediate hypotension, flushing, headache, vascular permeability
  • > H1 mediates coronary vasoconstriction, slows AV nodal conduction and bronchospasm
  • > H2 chronoptropy, ionotropy = tachycardia
  • tryptase
  • > relatively specific marker for mast cell degranulation
  • PAF
  • > bronchoconstriction
  • > vascular permeability
  • > chemotaxis
  • eicosanoids
  • > vasodilation
  • > vascular permeability
  • > bronchoconstriction (much more than histamine)
  • inflammatory cytokines
  • > drives delayed inflammatory response
  • > influx inflammatory cells
  • > mediator release acts directly on tissue causing allergic symptoms
  • > further recruitment of inflamm cells in vicious cycle
  • counter-regulatory mediators
  • > renin and chymase
  • > activation of RAS and angiotensin 2 formation
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10
Q

anaphylaxis diagnostic criteria

A

1

  • acute onset
  • mucocutaneous symptoms with
  • > resp symptoms
  • > decreased BP and its manifestations

2

  • exposure to likely allergen
  • any two of following
  • > mucocutaneous
  • > GI symptoms
  • > resp symptoms
  • > decreased BP and its manifestations

3

  • exposure to known allergen
  • decreased BP and its manifestations
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11
Q

anaphylaxis ddx

A

ASAP Fluids, Ventilation, Adrenaline

  • anaphylaxis sub types
  • shock
  • > septic
  • > cardiogenic
  • > hypovolemic
  • asthma/COPD exacerbation
  • panic attack
  • foreign body aspiration
  • vasovagal reaction
  • anaphylactoid reaction
  • > drugs
  • > contrast
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12
Q

anaphylaxis treatment

A

lie patient down

  • > sitting/standing up decreases venous return
  • > PEA
A
-patency
-angioedema 
B
-non rebreather 
-low threshold for intubate
->stridor
C
-two large IV canulas
->normal saline as fast as possible
-IM adrenaline
->1:1000 ampule into 1mL syringe
->max dose for adult = 0.5mg (half syringe)
->repeat every 5-15 mins
-IV adrenaline
->only when no response to several IM
->give as slow infusion not bolus
->1:10,000 syringe into 1L bag
->gives 1mcg/mL
->start at 1mcg/kg/min and increase
->safe upper limit unknown
D
-serially assess GSC
E
-remove allergen
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13
Q

late management anaphylaxis

A

Adjuvant pharm

  • bronchodilators
  • > SABAs
  • glucocorticoids
  • > methypred
  • > no evidence for use
  • > prevent biphasic reaction
  • antihistamines
  • > predominantly H1
  • > no role in acute treatment
  • > may relieve mucocutaneous symptoms

Time to discharge

  • usually 4 hours
  • biphasic can occur up to 72 hours after
  • > occurs in 20%

SAFE discharge

  • seek support
  • > education on anaphylaxis
  • > informing family and carers
  • > anaphylaxis emergency plan
  • allergen avoidance
  • follow up
  • > with immunologist
  • > allergy identification
  • > anaphylaxis diagnosis often changed
  • epinephrine
  • > two scripts
  • > urge to fill immediately
  • > educate on proper use
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14
Q

anaphylaxis investigations

A
ABG
-resp failure
-acidosis
->resp 
->mixed with lactate build up
ECG
FBC
EUC
-end organ damage
-GFR
LFTs
-end organ damage
tryptase
-early collection
-sensitive for anaphylaxis
plasma histamine
->peaks within 15mins
->baseline within 60mins
->can support anaphylaxis

consider:

  • CXR
  • > ddxs
  • trops
  • > MI as complication

later

  • in vitro IgE
  • > quantitate allergen specific IgE
  • skin test
  • > eg scratch test
  • > greater than 3cm
  • challenge
  • > avoid in anaphylaxis
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15
Q

chronic cholecystitis path

A

macroscopic

  • serosa is smooth and glistening
  • > covered with dense fibrous adhesions
  • wall
  • > variable thickness
  • > gray appearance
  • lumen
  • > greeny bile with gall stones

microscopic

  • subserosal fibrosis
  • mucosa
  • > macrophage, plasma cells, lymphocytes
  • > folds of mucosa with buried crypts
  • > outpouching of epithelium into walls (rokitansky aschoff sinus)
  • evidence of chronic complications
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16
Q

rheumatoid aetiology, pathophys

A

aetiology

  • genes
  • > HLADRB1 polymorphism
  • shared epitope
  • > disease associated alleles code for constant amino acid sequence in HLADRB1 chain termed shared epitope
  • > these alleles have worse disease outcomes
  • non-genetic
  • > ?EBV
  • > female
  • > 50-55
  • > smoking

pathophys

  • synovial CD4 T cells activated by APC
  • > mediate differentiation of B cells into autoantibody produces plasma cells
  • > fix complement within joint and drive inflammation
  • TNF α
  • > released by synovial macrophage and fibroblasts
  • > promotes inflammatory infiltrate
  • > stimulates osteoclastogenesis
  • > up-regulates DKK1->internalises Wnt
  • > Wnt decreases RANKL, increases OPG and activates osteoblasts
  • > increased RANKL expression
  • this is formation of pannus
  • > drives bone resorption at sites of synovial insertion
  • periarticular osteopenia
  • > likely due to inflammation within marrow
17
Q

pathology of rheumatoid joint

A

hallmarks of rheumatoid are

  • synovial inflammation (pannus)
  • focal bone erosion
  • > near synovial insertions
  • thinning of articular cartilage
  • peri-articular osteopenia

synovium

  • pannus
  • > hyperplasia of lining layer of synovium
  • > thickened cellular membrane
  • > contains fibroblast like synoviocytes and granulation reactive fibrovascular tissue
  • neo-angiogenesis
  • inflammatory infiltrate of lining layer
  • > CD4 T cells
  • > B cells
  • > macrophages
  • > randomly distributed or forming follicular structures

synovial fluid

  • culture
  • > sterile
  • microscopy
  • > turbid fluid
  • > raised WCC
  • > polymorphs
  • > no crystals
  • complement levels
  • > decreased
  • biochem
  • > protein increased
  • > glucose decreased
18
Q

pathology rheumatoid nodules

A

usually found on extensor surfaces
->due to immune complex deposition

morphology-

  • central area of necrosis
  • surrounded by palisading macrophages and then lymphocytes
  • focal vasculitis
  • > with Ig and fibrin deposition
19
Q

clinical course, joint and systemic complications rheumatoid

A

joint

  • pain
  • stiffness
  • loss of function
  • > reduced grip strength
  • > wasting of intrinsic hand muscles
  • tenosynovitis
  • > trigger finger
  • > tendon rupture
  • swelling
  • > carpal tunnel
  • deformity
  • > ulnar deviation/volar subluxation
  • > swan neck/boutonniere/z thumb

systemic (part of autoimmunity and immune complex dep)

  • eyes
  • > sicca syndrome
  • > episcleritis/scleritis
  • neck
  • > atlanto-axial disease
  • lungs
  • > rheumatoid pleurisy
  • cardiac
  • > pericarditis
  • > MI
  • renal
  • > membranous nephropathy
  • skeletal
  • > osteoporosis
  • skin
  • > nodules
  • blood
  • > anaemia
  • > feltys
  • > DLBC lymphoma
  • endocrine
  • > hypogonadism

course

  • 10% undergo remission within 6 months
  • the rest
  • > progressive, waxing and waning illness
  • a few
  • > recurrent attacks with periods of quiescence
  • gradual increase in disability
  • > 50% unable to work after 10 years
  • mortality
  • > 2x general
  • > shortened life expectancy by approx 5 years
  • > MI most common cause of death