Medicine (10) Flashcards
What’s Sjogren’s syndrome? (pathophysiology)
- lymphocytic infiltration of exocrine glands
- predominantly lacrimal and salivary glands → dry eyes, dry mouth
Demographics of Sjogren’s syndrome
- primary or secondary (to RA or other)
- predominantly females (9:1)
- marked increased risk of lymphoid malignancy (40-60 fold)
Presenting symptoms in Sjogren’s syndrome
- Dryness of: eyes, mouth, respiratory tract, vagina
- Arthritis
- lymphademopathy
- gland swelling
Ix in suspected Sjogren’s syndrome
- Anti-Ro and Anti-La
- RF positive in most cases (>99%)
- Schirmer’s test (filter paper to measure tear formation)
Management of Sjogren’s syndrome
- Artificial tears and moistening spray
- Pilocarpine (stimulate saliva production)
- NSAIDs
- DMARDs (if needed)
(2) Large vessel vasculitis (conditions)
- Giant Cell Arteritis
- Takayasu
(2) Medium vessel vasculitis (conditions)
- Kawasaki
- Polyarthritis Nodosa
(2) subclasses of small vessel vasculitis
- ANCA +ve (Microscopic polyangiitis, Churg-Strauss syndrome, Wegener’s)
- ANCA -ve (Good Pasture, Henoch-Schonlein)
ANCA -ve conditions (2)
Small vessel ANCA -ve conditions:
- Goodpasture
- Henoch-Schonlein Purpura
ANCA +ve small vasculitis conditions (3)
- Microscopic polyangiitis (p-ANCA)
- Churg-Strauss (p-ANCA)
- Wegener’s (c-ANCA)
Giant Cell Arteritis/ Polymyalgia Rheumatica
- symptoms of both
- Ix
- Management
Takayasu arteritis
- symptoms
- treatment
Polyarteritis Nodosa
- what happens
- presentation
- association
- management
Pathophysiology: Rare necrotizing vasculitis that involves many
organs
Presentation depends on organ involved but
can be dramatic due to infarction:
- Myocardial Infarction
- Haematuria
- Abdominal pain
Association: with Hepatitis
Management: corticosteroids and immunosuppresants
Classification of glomerulonephritis (2)
- NephrOtic Syndrome
- Nephritic Syndrome
Triad and associations with nephrotic syndrome
NephrOtic syndrome
Triad of:
- PrOteinuria
- HypOalbuminaemia
- Oedema
Associated with hyperlipidaemia, reduced immunity and hypercoagulability
The most common cause of nephrotic syndrome (in adults and in children)
The most common:
- Adults → diabetic nephropathy
- Children → minimal change disease
Membranous GMN
- what type of glomerulonephritis
- cause
- association
- what happens
Membranous glomerulonephritis → nephrotic syndrome
- idiopathic
- associated with SLE and hepatitis
- Pathophysiology: thick glomerular basement membrane
Focal segmental glomerulonephritis
- type of glomerulonephritis
- cause
- association
- what happens (simple pathophysiology)
Focal segmental GMN → nephrotic syndrome
- idiopathic
- associated with HIV
Pathophysiology: effacement of foot processes of podocytes
*Focal Segmental GMN does not respond to steroids
Pathophysiology of diabetic nephropathy
*what drug to use and why
- ↑ glucose → non-enzymatic glycosylation of vascular basement membrane → hyaline arteriosclerosis
- Efferent arteriole more affected → hyperfiltration
- Hyperfiltration injury leads to micoalbuminuria
ACE inhibitors slow the progression of hyperfiltration-induced damage
(as Angiotension II causes vasoconstriction of the efferent arteriole)
Triad of Nephritic syndrome
1. Proteinuria
2. Haematuria
3. Fluid overload (acute)
Brown/Coca-cola urine
The most common cause of nephritic syndrome in adults and kids
Adults → IgA nephropathy
Children → post-streptococcal glomerulonephritis
Other (than the most common) causes of nephritis syndrome
Most common:
- adults → IgA nephropathy
- kids → post-streptococcal GMN
- Crescentic GMN
- Goodpasture’s syndrome (anti-GBM)
- Diffuse proliferative GMN (SLE)
- Alport syndrome (congenital deafness)
- Vasculitis (GPA, Churg-Strauss)
Causes of AKI
(4) problems that AKI causes
- Uraemia
- Failure of fluid balance (fluid overload)
- Fluid of electrolyte regulation (K+↑↑)
- Failure of acid-base regulation (acidosis)
Investigations in AKI
Bedside – Urinalysis + Culture (Infection, protein, blood). ECG (?arrhythmias)
Bloods – FBC (infection), U&Es (renal function, K+), Blood Cultures & lactate (if sepsis suspected), ABG (metabolic acidosis), autoantibody
screen (ANA, ANCA, Anti-GBM)
Imaging – Ultrasound (exclude obstruction and assess renal size), CXR (pulmonary oedema due to fluid overload)
Invasive – Biopsy (if renal cause suspected)
Treatment of AKI
(4) ECG signs of hyperkalaemia
- Low flat P waves
- Broad Bizarre QRS
- Slurring into the ST segment
- Tall Tented T-waves
Management of hyperkalaemia
- IV Calcium Gluconate 10% in 10ml
- ActRapid 10 Units + Glucose 50% in 50ml
- Salbutamol 10mg NEB
- Calcium Resonium
- Dialysis
