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Lancaster FINALS _slide > Medicine (10) > Flashcards

Medicine (10) Flashcards

1
Q

What’s Sjogren’s syndrome? (pathophysiology)

A
  • lymphocytic infiltration of exocrine glands
  • predominantly lacrimal and salivary glands → dry eyes, dry mouth
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2
Q

Demographics of Sjogren’s syndrome

A
  • primary or secondary (to RA or other)
  • predominantly females (9:1)
  • marked increased risk of lymphoid malignancy (40-60 fold)
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3
Q

Presenting symptoms in Sjogren’s syndrome

A
  • Dryness of: eyes, mouth, respiratory tract, vagina
  • Arthritis
  • lymphademopathy
  • gland swelling
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4
Q

Ix in suspected Sjogren’s syndrome

A
  • Anti-Ro and Anti-La
  • RF positive in most cases (>99%)
  • Schirmer’s test (filter paper to measure tear formation)
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5
Q

Management of Sjogren’s syndrome

A
  • Artificial tears and moistening spray
  • Pilocarpine (stimulate saliva production)
  • NSAIDs
  • DMARDs (if needed)
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6
Q

(2) Large vessel vasculitis (conditions)

A
  • Giant Cell Arteritis
  • Takayasu
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7
Q

(2) Medium vessel vasculitis (conditions)

A
  • Kawasaki
  • Polyarthritis Nodosa
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8
Q

(2) subclasses of small vessel vasculitis

A
  • ANCA +ve (Microscopic polyangiitis, Churg-Strauss syndrome, Wegener’s)
  • ANCA -ve (Good Pasture, Henoch-Schonlein)
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9
Q

ANCA -ve conditions (2)

A

Small vessel ANCA -ve conditions:

  • Goodpasture
  • Henoch-Schonlein Purpura
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10
Q

ANCA +ve small vasculitis conditions (3)

A
  • Microscopic polyangiitis (p-ANCA)
  • Churg-Strauss (p-ANCA)
  • Wegener’s (c-ANCA)
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11
Q

Giant Cell Arteritis/ Polymyalgia Rheumatica

  • symptoms of both
  • Ix
  • Management
A
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12
Q

Takayasu arteritis

  • symptoms
  • treatment
A
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13
Q

Polyarteritis Nodosa

  • what happens
  • presentation
  • association
  • management
A

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

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14
Q

Classification of glomerulonephritis (2)

A
  • NephrOtic Syndrome
  • Nephritic Syndrome
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15
Q

Triad and associations with nephrotic syndrome

A

NephrOtic syndrome

Triad of:

  1. PrOteinuria
  2. HypOalbuminaemia
  3. Oedema

Associated with hyperlipidaemia, reduced immunity and hypercoagulability

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16
Q

The most common cause of nephrotic syndrome (in adults and in children)

A

The most common:

  • Adults → diabetic nephropathy
  • Children → minimal change disease
17
Q

Membranous GMN

  • what type of glomerulonephritis
  • cause
  • association
  • what happens
A

Membranous glomerulonephritis → nephrotic syndrome

  • idiopathic
  • associated with SLE and hepatitis
  • Pathophysiology: thick glomerular basement membrane
18
Q

Focal segmental glomerulonephritis

  • type of glomerulonephritis
  • cause
  • association
  • what happens (simple pathophysiology)
A

Focal segmental GMN → nephrotic syndrome

  • idiopathic
  • associated with HIV

Pathophysiology: effacement of foot processes of podocytes

*Focal Segmental GMN does not respond to steroids

19
Q

Pathophysiology of diabetic nephropathy

*what drug to use and why

A
  • ↑ 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)

20
Q

Triad of Nephritic syndrome

A

1. Proteinuria

2. Haematuria

3. Fluid overload (acute)

Brown/Coca-cola urine

21
Q

The most common cause of nephritic syndrome in adults and kids

A

Adults → IgA nephropathy

Children → post-streptococcal glomerulonephritis

22
Q

Other (than the most common) causes of nephritis syndrome

A

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)
23
Q

Causes of AKI

A
24
Q

(4) problems that AKI causes

A
  1. Uraemia
  2. Failure of fluid balance (fluid overload)
  3. Fluid of electrolyte regulation (K+↑↑)
  4. Failure of acid-base regulation (acidosis)
25
Q

Investigations in AKI

A

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)

26
Q

Treatment of AKI

A
27
Q

(4) ECG signs of hyperkalaemia

A
  1. Low flat P waves
  2. Broad Bizarre QRS
  3. Slurring into the ST segment
  4. Tall Tented T-waves
28
Q

Management of hyperkalaemia

A
  1. IV Calcium Gluconate 10% in 10ml
  2. ActRapid 10 Units + Glucose 50% in 50ml
  3. Salbutamol 10mg NEB
  4. Calcium Resonium
  5. Dialysis

Lancaster FINALS _slide (31 decks)

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