Last Minute Bits Flashcards

(56 cards)

1
Q

CKD Measuring Proteinuria

A

> 3= Proteinuria basically in EARLY MORNING

3-70= Repeat the sample

> 70= No need to repeat

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2
Q

When to Refer to a Nephrologist in Proteinuria in CKD

A

if >70

if >30 with Haematuria

if >3 with Haematuria and CVD/ lowering eGFR

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3
Q

When to start the ACE, sGLT2 and Statins for Proteinuria in CKD

A

if ACR>70

if HTN and ACR>30

if Diabetes and ACR>3

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4
Q

Why might a patient not respond to EPO?

A

Aluminium Toxicity
Iron Deficiency (so correct Iron First/ Measure Iron Levels first)
High Parathyroid

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5
Q

What is Type 1 and Type 2 Renal Tubular Acidosis?

A

Type 1= DCT

Type 2= PCT (Fanconi Syndrome)

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6
Q

When should you suspect Focal Segmental Glomerulosclerosis?

A

Minimal Change Disease that is NOT responding to steroids

Patient has Sickle Cell/ Alports Syndrome/ HIV/ is a Drug Addict

Also Parvovirus if they have Sickle Cell

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7
Q

What investigations should be checked in Haematuria?

A

Urine Dipstick

Blood Pressure

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8
Q

When should Haematuria be referred? (2ww)

A

> 45 years old with no sign of UTI

> 60 years old with Dysuria or a raised WCC

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9
Q

Investigations in HUS

A

Stool Culture
FBC for Anaemia
Blood Film for Schistocytes

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10
Q

What is the pathophysiology and management of IgA Nephropathy

A

IgA deposition in Mesangium

Proteinuria <500= No Rx Needed

Proteinuria >500= ACE and Steroids

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11
Q

What is seen in Rapidly Progressive Glomerulonephritis?

A

Cresenteric GN

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12
Q

What types of Antibodies are seen in PSGN?

A

IgG/ IgM

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13
Q

What is the blood investigations for PSGN? and why may it be normal despite the patient actually having PSGN?

A

Anti-Streptolysin O

Normal due to HIGH CHOLESTEROL LEVES

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14
Q

How does Nephrotic Syndrome affect the Thyroid Levels?

A

It lowers the TOTAL

but not the FREE Thyroxine Levels

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15
Q

In cells, What comes out with Potassium out of channels, and what goes in through channels?

A

Potassium Out
Water Out

H+ IN

Also other way around

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16
Q

What are the Signs of Hypokalaemia?

A

Less Stools
Lots of Urine

Leg Cramps
Limp Muscles

Lethargy

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17
Q

What are the causes of Hypokalaemia?

A

GRAPHIC IDEA

GI Loss
Renal Tubular Acidosis
Aldosterone
Paralysis
Hypothermia
Insulin
Cushing’s

Intake is not enough
Diuretics
Elevated SABA use
Alkalosis

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18
Q

What are two things that can cause High Aldosterone?

A

Compensated Heart Failure
Cirrhosis

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19
Q

What is seen in Type 1 and Type 2 Membranoproliferative Glomerulonephritis

A

Type 1 activates Classic Complement
- Causes are- Cryoglobuminaemia and Hepatitis C

Type 2 activates Alternative Complement
- causes are Factor H Deficiency, Partial Lipodystrophy, Low Circulating C3

STEROIDS may be used to manage Membranoproliferative Glomeruolonephritis

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20
Q

What causes Membranous Glomerulonephritis (the COMMONEST Glomerulonephritis in Adults)?

A

A Lot of INFECTIONS, and INFLAMMATORY REACTIONS
Also MALIGNANCY

Also Gold and Penicillamine

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21
Q

How do you manage Membranous Glomerulonephritis?

A

ACE/ ARBs

If Severe- Manage as Diffuse Proliferative (Steroids and Cyclophosphamide)

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22
Q

Peritoneal Dialysis can cause Peritonitis due to Staph Epidermis- how do you manage this?

A

Vancomycin added to Dialysis Fluid

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23
Q

What are the 3 Nephritic Syndromes?

A

IgA

Alports

Rapidly Progressive

24
Q

What is one of the biggest risks of Rapidly Progressive Glomerulonephritis?

A

Clotting due to HIGH FIBRIN LEVELS

25
What is the management of Rapidly Progressive Glomerulonephritis?
Anticoagulants Plasmapharesis *ImmunoSuppressants* Dialysis
26
How long does it take for an AV Fistula to form?
6-8 weeks
27
What are the Complications of Haemodialysis?
Cardiac Arrhythmia Hypotension Anaphylactic Reaction Site Infection Endocarditis
28
What are the side effects of Peritoneal Dialysis?
Constipation Peritonitis Back Pain Hyperglycaemia
29
What are the side effects of Renal Transplant?
DVT/ PE Malignancies (Squamous Cell Carcinoma due to immunosuppressant use and Lymphoma) Recurrence of Original Disease Rejection
30
What type of reaction is Hyperacute Rejection?
Type 2 due to preexisting antibodies
31
What is Acute Rejection?
Type 4 Due to HLA Mismatch/ CMV Infection Manage with Steroids and Immunosuppressants
32
What is Chronic Rejection?
usually due to the Recurrence of the original Disease
33
How is GvHD managed?
IV Steroids
34
What suggests Rhabdomyolysis
HIGH P's and Low C High Potassium and Phosphate and Low Calcium And CK higher that 5 times the upper limit of normal
35
How is Rhabdomyolysis managed?
JUST Iv Fluids and Alkalise the Urine
36
What are HYALINE CASTS in URINE?
Tamm-Horsfall Proteins Seen in Exercise and Loop Diuretic Use
37
What is the URINE Osmolality in PRE and INTRA renal AKI?
Pre- >500 as it is trying to increase blood pressure to make up for fluid loss Intra- <350
38
How is Alports managed?
ACE/ ARBs for the Proteinuria and Lens Replacement for the LENS Issues
39
Management of Closed Angle Glaucoma
Pilocarpine Timolol Apraclonidine (a2 agonist- avoid MAOIS and TCAs) Acetazolamide
40
Closed and Open Angle Glaucoma vs Long and Short Sightedness
Closed- LONG SIGHTEDNESS Open- SHORT SIGHTEDNESS
41
Management of Open angle Glaucoma
If IOP>24= 360 SLT Prostaglandins Then same management as Closed Angle
42
How is Blepharitis managed?
It can have Styes and Chalazions so manage it the same as those with Hot Compresses and eyelid hygeine
43
Causes of CRVO
PHADO Polycythaemia Hyprtension Arteriosclerosis Diabetes Obesity
44
Management of CRVO
CRVO- Conservative Macular Oedema= Anti VEGF Retinal Neovascularisation= Laser Photocoagulation
45
Management of CRAO
Treat the underlying cause and IntraArterial Thrombolysis
46
When is a RAPD seen?
Anything that affects the optic nerve or affects blood supply to the retina so MS and CRAO
47
What is the management of Conjunctivitis in pregnant women?
Fusidic Acid
48
What is the 4,2,1 rule for categorising Severe Non-Proliferative Diabetic Retinopathy
Severe if: Haemorrhages or Microaneurysms (small red dots) seen in all 4 quadrants or Venous beading in 2 or more quadrants or IRMA appears in at least 1 quadrant
49
What is the difference between superficial and deep haemorrhages
Superficial= Flame Haemorrhages Deep= BLOT/ DOT
50
Where are Hard Exudates usually found?
In the Macular (can present as CIRCINATE pattern or MACULAR STAR pattern)
51
What are IRMAs?
They are small blood vessels that arise from capillaries and look like lil hairs in between the actual big vessels These are different from NEOVASCULARISATION- where the blood vessels are NOT connected to a capillary and just form out of the blue
52
What defines Mild NPDR in Diabetic Retinopathy
Ther will ONLY be microaneurysms and nothing else
53
How is NPDR managed?
If Severe= Panretinal Laser Photocoagulation
54
How is Proliferative Diabetic Retinopathy managed?
Panretinal Laser Photocoagulation AntiVEGF Vitroretinal Surgery
55
What are the stages of Hypertensive Retinopathy?
Stage 1- Narrowing of Arterioles and Increased Light Reflex (makes it look like SILVER WIRES) Stage 2- AV Nipping Stage 3- Cotton Wool Exudates and Flame Haemorrhages Stage 4- Papilloedema
56
Red EYE Classification?
Painless and Normal Vision= Conjunctivitis Painless and Blurred Vision- Anterior Uveitis (rare) Painful and Blurred Vision- Also Anterior Uveitis/ Keratitis/ Glaucoma - vision is worse in uveitis than keratitis Photophobia- Uveitis and Keratitis Haloes- Glaucoma Pupil= Small in Uveitis/ Big in Glaucoma