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Medicine year 4 CDM > Block 4: extra > Flashcards

Block 4: extra Flashcards

1
Q

What is pre-emptive transplantation in CKD

A

Look for a potential living donor to do the transplant before the person progresses to end stage disease (best treatment, has better outcomes)

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2
Q

What gene is affected in the majority of Alport syndrome

A

Collagen 4a5 (encodes for a collagen protein present in the basement membrane of the glomerulus and basement membranes in the inner ear and eye)

Phenotype: Glomerular disease with hematuria and proteinuria, early onset sensorineural deafness and can get an eye condition called anterior lenticonus (which is pathognomonic of this condition)

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3
Q

Treatment of diabetic nephropathy complications

A

Proteinuria: ACEi/ARB or SGLT2

Renal bone disease: activated vitamin D, phosphate restricted diet, phosphate binders and Ca supplementation

Secondary hyperparathyroidism: active vit D, phosphate binders and phosphate restricted diet

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4
Q

What eGFR affects drug dosing

A

<30

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5
Q

Contrast induced nephropathy

A

A 25% increase in serum creatinine (SCr) from baseline, or a 0.5 mg/dL (44 µmol/L) increase in absolute SCr value, within 48-72 hours after intravenous contrast administration

Arterial phase contrast i.e. used in PCI is the most nephrotoxic

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6
Q

Symptoms experienced during dialysis

A

Dizziness, presyncope, cramps and fatigue (need to adjust rate)

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7
Q

What is the kidney sharing scheme

A

Patients register a potential live donor who is willing to donate a kidney but they are not a HLA match with the patient. Then matching runs identify multi way exchanges (eg. 2 way or 3 way exchanges), short altruistic donor chains and long altruistic donor chains

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8
Q

What is done after a kidney transplant

A
  • A ureteric stent which may be removed after 6 weeks
  • Immunosuppression : Tacrolimus, MMF (myocphenolate mofetil) and prednisolone
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9
Q

Mesangial IC deposition in GN

A

Function is usually well preserved initially but leads tomesangioproliferative glomerulonephridites (e.g. IgA nephropathy- most common primary cause and class II lupus nephropathy) and tends to lead to stable or slowly progressive renal impairment (typically causes CKD)

Immune cascade tends to be more aggressive as its in close contact to the blood

Causes: stable or slowly progressive renal impairment (CKD)

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10
Q

IC deposition in the subendothelial space in GN

A
  • More aggressive as in close contact to the blood
  • Causes abrupt fall in GFR= AKI, typically causes nephritic syndrome
  • Causes rapid progressive glomerulonephritis
  • On biopsy see glomerular damage, fragmentation of glomerular tuft and capsule with hypercellular bowmans capsule (immune complexes deposited). Cescenteric GN, basement membrane rupture in RPGN (leaks blood and protein)
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11
Q

IC in subepithelial space

A

Still close enough to the blood to trigger an immune cascade, complement components directly injure epithelial cells but there is less recruitment of other inflammatory mediators= non-inflammatory damage of epithelial cells

Protein leak due to damage to the podocytes and GBM

Can occur in Membranous glomerulonephritis and class V lupus nephritis (nephrotic syndrome)

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12
Q

Different types of injury in GN

A
  • Epithelial injury: nephrotic range proteinuria and non-inflammatory lesions
    -Endocapillary injury: haematuria, loss of GFR, proteinuria and inflammatory lesions, rapid AKI
  • Mesangial injury: asymptomatic proteinuria and microscopic haematuria
  • Glomerulus: nephrotic and nephritic syndrome
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13
Q

GFR in nephritic and nephrotic syndrome

A

Always reduced in nephritic syndrome, often preserved in nephrotic

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14
Q

What proteins are lost in the urine in nephrotic syndrome

A

Antithrombin III (prothrombotic- risk of clots), transferrin (anaemia) and immunoglobulins (immunodeficient- issue in paeds, fluid in ascites can become infected= spontaneous bacterial peritonitis)

Causes: Elevated cholesterol, proteinuria (>3g/24hr), hypoalbuminaemia, reduced transferrin/Hb, oedema, thromboembolic complications, risk of immunodeficiency

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15
Q

How does diabetic nephropathy present

A

Low level albuminuria with glomerular hyperfiltration and increased GFR followed by increasing albuminuria often in the nephrotic range with a progressive decline in GFR

Microscopically: Kimmelsteil-Wilson nodule (from mesangial expansion) with thickened GBM

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16
Q

What are the clinical features of lupus (4 needed for diagnosis- at least 1 clinical + 1 lab finding)

A

Clinical: Acute cutaneous lupus, chronic cutaneous lupus, oral/nasal ulcers, non-scarring alopecia, arthritis, serositis, renal, neurologic, haemolytic anaemia, leukopenia and thrombocytopenia.

Lab findings: ANA, anti-DNA, anti-SM, antiphospholipid AB, low complement (C3, C4, CH50), direct Coombs test

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17
Q

The immunological criteria for SLE

A

Anti-nuclear, anti-DNA, and-Sm, anti-phospholipid, low complement C3, C4, CH50, and direct Coombe’s test

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18
Q

When do you start dialysis

A

If eGFR <10

Urgently: Severe metabolic acidosis, life-threatening pulmonary oedema, resistant hyperkalaemia, uraemic pericarditis or uraemic encephalopathy

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19
Q

AV fistula versus Central venous dialysis catheter

A

AV fistula: connection between brachial artery and cephalic vein. Needs to develop for 6 weeks

Central venous dialysis catheter (used in urgent haemodialysis, risk of stenosis and high risk of infection)

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20
Q

The 2 classes of HLA

A

MHC-I (on antigen presenting cells allowing presentation of CD-8 cells. HLA-A, HLA-B and HLA-C

MHC-II (on antigen presenting cell allowing activation of DC-4 cells). HLA-DR, HLA-DQ and HLA-DP

21
Q

What is HLA matching based on

A

Matching 3 haplotypes- A, B and DR (the perfect match is if all of these line up the same= 0,0,0 mismatch)

The HLA matches which allow renal transplantation: 0,0,0 and 0,0,1 and 1,1,1

22
Q

Diuretics in renal impairment

A

In reduced eGFR a loop diuretic is the recommended type

Don’t use thiazide diuretics if <30 eGFR

23
Q

Medicationsto stop in CKD

A

Avoid NSAID’s, can use asprin in CVD
Avoid codeine and morphine
Stop Metformin in renal impairment

24
Q

Scoring system for NAFLD

A
  • NAFLD Fibrosis Score (NFS) — an intermediate or high score (greater than minus 1.455), suggests advanced liver fibrosis.
  • Fibrosis (FIB)-4 Score (FIB-4) — a score of greater than 2.67 suggests advanced liver fibrosis.
  • Enhanced Liver Fibrosis (ELF) test — a score of 10.51 or above suggests advanced liver fibrosis.
25
Q

Contraindications for liver transplant

A
  • Significant co-morbidities (e.g., severe kidney, lung or heart disease)
  • Current illicit drug use
  • Continuing alcohol misuse (generally 6 months of abstinence is required)
  • Untreated HIV
  • Current or previous cancer (except certain liver cancers)
26
Q

Types of liver transplant

A
  • Orthotopic transplant: healthy person that has just died, entire liver
  • Living donor transplant: when a portion of the liver is taken from a living donor
  • Split donation: when a deceased persons liver is split in two and given to two different people
27
Q

Summary of secondary causes of obesity

A
  • Endocrine: Cushing’s, Hypothyroidism, Acromegaly, Pseudo hypoparathyroidism
  • Genetic: Prader-willi, Bardet-Biedel syndrome, Cohen syndrome
  • CNS: Hypothalamic tumour, trauma or inflammation
28
Q

Investigations in obesity

A

Plasma Urea, Electrolytes
HbA1c
Thyroid function tests
Overnight Dexamethasone suppression Test-To rule out Cushing’s syndrome
Plasma IGF-1 to rule out Acromegaly
BMI

29
Q

Causes of secondary hyperlipidaemia

A
  • Diabetes
  • Alcoholism
  • Hypothyroid
  • Nephrotic syndrome
  • Chronic renal failure
  • Pregnancy
30
Q

Initial tests in hypertension

A

Check the pulse
Repeat the blood pressure recording adopting best practice
Do a cardiovascular examination
Fundoscopy
U&E’s, eGFR, urine albumine:creatinine ratio and urine dip- check for kidney damage
HbA1C
12 lead ECG
Lipid screen

31
Q

Conditions which cause secondary hypertension

A
  • Renal: Glomerulonephritis, pyelonephritis, adult PCKD, renal artery stenosis
  • Endocrine: Phaeochromocytoma, Cushing’s syndrome, Acromegaly, congenital adrenal hyperplasia
  • Drugs: steroids, MAOI’s, COCP, NSAID’s, Leflunomide
  • Other: pregnancy, coarctation of the aorta
32
Q

First line investigations in PAD

A
  • Bedside: cardiovascular risk assessment, ECG, BP, Buerger’s test, ABPI
  • Bloods: FBC, HBa1c, full lipid screen, U&E’s
  • Imaging: duplex scan for pulses, cross sectional imaging (CT or MRI) when there is no femoral pulse
33
Q

ABPI

A
  • The lower it is the worst the PAD is
  • <0.9 is diagnostic
  • Calcification of arteries gives abnormally high score so may skew results.Diabetes can skew results
34
Q

PAD

A
  • Pathology: arterial supply of oxygen and nutrients to legs reduced, usually due to atherosclerosis
  • Risk factors: Hypertension, smoking, diabetes mellitus, hyperlipidaemia, old age, obesity
  • Symptoms: intermittent claudication pain
  • Complications: critical limb ischaemia, gangrene
  • Appearance: cool, pale foot, increased CRT, thin and shiny skin with poor nail/hair growth
  • Treat with modifying risk factors, statins and graded exercise programme
35
Q

Venous disease

A
  • Pathology: venous drainage of the legs poor, usually sue to vein wall/valve damage or reduced calf movement
  • Risk factors: female, old age, prolonged standing, physical inactivity, previous DVT
  • Symptoms: asymptomatic, deep aching discomfort, heaviness, itch
  • Complications: varicose veins, venous ulcers, oedema, venous eczema, DVT
  • Appearance: oedema, telangiectasia, malleolar flare, brown haemosiderin deposits, dilated veins
  • Treat with compression bandages
36
Q

Acute limb ischaemia and critical limb ischaemia

A

Acute limb ischaemia: An acute loss of blood supply, often due to acute occlusion. Symptoms are present <2 weeks. This is a time-critical emergency.

Critical limb ischaemia: Progression of peripheral arterial disease to the point that cells have insufficient blood supply. Defined by intractable rest pain of >2 weeks, gangrene or non-healing ulceration.

37
Q

Management of acute limb ischaemia

A
  • Arrange for urgent admission to hospital for assessment
  • Initial assessment with ABCDE approach
  • Bloods including coagulation and G&S for potential surgery
  • Initial doppler US at the bedside, then CT angiogram
  • The Rutherford score may be used to determine if leg is viable
  • IV Heparin infusion is started
  • Surgical options include: thrombolysis, embolectomy, bypass surgery
  • Amputation if limb is deemed non-viable and ischaemia is irreversible
38
Q

Initial investigations for breathlessness

A

Bedside: ECG, spirometry (if suspect COPD), urine sip +/- urinalysis
Bloods: FBC, U&Es, TSH, NT-Pro-BNP
Imaging: Chest Xray

39
Q

HFrEF vs HFpEF

A

HF with reduced ejection fraction: Ejection fraction is ≤40%. Primarily an issue of systolic function, with impaired ability of the ventricle to pump blood out.

HF with preserved ejection fraction: Heart failure due to impaired ventricle filling during diastole. Ejection fraction is normal or very mildly impaired (LV ejection fraction >50%

The European Society of Cardiology have recently introduced a new category of Heart Failure with mildly reduced ejection fraction (HFmrEF)- Ejection fraction 41-49%

40
Q

Initial approach to acute heart failure

A
  • ABCDE assessment of the patient – give oxygen to correct hypoxia and sit upright
  • Intravenous diuretics (e.g. furosemide) should be given immediately to relieve pulmonary oedema
  • Once stabilized the patient should be monitored with daily observations, measurement of fluid balance (eg with daily fasting weight) and close monitoring of renal function (daily Urea and Electrolyte measurement)
    y
41
Q

CXR in silicosis

A
  • Multiple and small well-rounded nodules, particularly in the upper zone.
  • Apical hilar retraction
  • Secondary TB infection in apical cavities
  • Predisposes patients to TB
  • Hilar egg-shell calcification
42
Q

When vocal resonance is increased or decreased

A

Vocal resonance is increased in consolidation(solid material) and REDUCED in pneumothorax(air).

43
Q

Fibrosis which affects the upper zones

A

hypersensitivity pneumonitis (also known as extrinsic allergic alveolitis)
coal worker’s pneumoconiosis/progressive massive fibrosis
silicosis
sarcoidosis
ankylosing spondylitis (rare)
histiocytosis
tuberculosis
radiation-induced pulmonary fibrosis

44
Q

Fibrosis which affects the lower zones

A

idiopathic pulmonary fibrosis
most connective tissue disorders (except ankylosing spondylitis) e.g. SLE
drug-induced: amiodarone, bleomycin, methotrexate
asbestosis

45
Q

TLCO and KCO in restrictive lung disease

A
  • Intra-pulmonary: TLCO and KCO reduced
  • Extra-pulmonary: TLCO reduced and KCO elevated
46
Q

Causes of erythema nodosum

A

Infections - Strep, TB, viruses
Drugs - amoxicillin, OCP
IBD
Sarcoidosis
Pregnancy
Behcets
Malignancy
Haematological malignancy

47
Q

Side effects of corticosteroids

A

Weight gain
Hypertension
Change in appearance
Skin changes
Hyperglycaemia
GI bleeding
Osteoporosis
Adrenal crisis (if dose missed or sick days)

48
Q

Investigations for pulmonary fibrosis

A

High resolution CT
Hx for potential cause - connective tissue disease, occupational Hx, pets/birds/hobbies
Bloods - auto antibodies Eg. RF, CK, ANA

49
Q

Advantages and disadvantages of lung biopsy

A

Advantages - allows absolute certainty of diagnosis

Disadvantages - post thoracotomy pain, pneumothorax, bleeding, infection

Medicine year 4 CDM (44 decks)

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