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Jan Stuff > Last Minute Bits > Flashcards

Last Minute Bits Flashcards

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
Q

What is the management of Rapidly Progressive Glomerulonephritis?

A

Anticoagulants
Plasmapharesis
ImmunoSuppressants
Dialysis

26
Q

How long does it take for an AV Fistula to form?

A

6-8 weeks

27
Q

What are the Complications of Haemodialysis?

A

Cardiac Arrhythmia
Hypotension
Anaphylactic Reaction
Site Infection
Endocarditis

28
Q

What are the side effects of Peritoneal Dialysis?

A

Constipation
Peritonitis
Back Pain
Hyperglycaemia

29
Q

What are the side effects of Renal Transplant?

A

DVT/ PE
Malignancies (Squamous Cell Carcinoma due to immunosuppressant use and Lymphoma)
Recurrence of Original Disease
Rejection

30
Q

What type of reaction is Hyperacute Rejection?

A

Type 2

due to preexisting antibodies

31
Q

What is Acute Rejection?

A

Type 4

Due to HLA Mismatch/ CMV Infection

Manage with Steroids and Immunosuppressants

32
Q

What is Chronic Rejection?

A

usually due to the Recurrence of the original Disease

33
Q

How is GvHD managed?

A

IV Steroids

34
Q

What suggests Rhabdomyolysis

A

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
Q

How is Rhabdomyolysis managed?

A

JUST Iv Fluids

and Alkalise the Urine

36
Q

What are HYALINE CASTS in URINE?

A

Tamm-Horsfall Proteins

Seen in Exercise and Loop Diuretic Use

37
Q

What is the URINE Osmolality in PRE and INTRA renal AKI?

A

Pre- >500 as it is trying to increase blood pressure to make up for fluid loss

Intra- <350

38
Q

How is Alports managed?

A

ACE/ ARBs for the Proteinuria and Lens Replacement for the LENS Issues

39
Q

Management of Closed Angle Glaucoma

A

Pilocarpine
Timolol
Apraclonidine (a2 agonist- avoid MAOIS and TCAs)
Acetazolamide

40
Q

Closed and Open Angle Glaucoma vs Long and Short Sightedness

A

Closed- LONG SIGHTEDNESS
Open- SHORT SIGHTEDNESS

41
Q

Management of Open angle Glaucoma

A

If IOP>24= 360 SLT

Prostaglandins

Then same management as Closed Angle

42
Q

How is Blepharitis managed?

A

It can have Styes and Chalazions so manage it the same as those

with Hot Compresses and eyelid hygeine

43
Q

Causes of CRVO

A

PHADO

Polycythaemia
Hyprtension
Arteriosclerosis
Diabetes

Obesity

44
Q

Management of CRVO

A

CRVO- Conservative

Macular Oedema= Anti VEGF
Retinal Neovascularisation= Laser Photocoagulation

45
Q

Management of CRAO

A

Treat the underlying cause and IntraArterial Thrombolysis

46
Q

When is a RAPD seen?

A

Anything that affects the optic nerve or affects blood supply to the retina

so MS and CRAO

47
Q

What is the management of Conjunctivitis in pregnant women?

A

Fusidic Acid

48
Q

What is the 4,2,1 rule for categorising Severe Non-Proliferative Diabetic Retinopathy

A

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
Q

What is the difference between superficial and deep haemorrhages

A

Superficial= Flame Haemorrhages

Deep= BLOT/ DOT

50
Q

Where are Hard Exudates usually found?

A

In the Macular (can present as CIRCINATE pattern or MACULAR STAR pattern)

51
Q

What are IRMAs?

A

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
Q

What defines Mild NPDR in Diabetic Retinopathy

A

Ther will ONLY be microaneurysms and nothing else

53
Q

How is NPDR managed?

A

If Severe= Panretinal Laser Photocoagulation

54
Q

How is Proliferative Diabetic Retinopathy managed?

A

Panretinal Laser Photocoagulation

AntiVEGF

Vitroretinal Surgery

55
Q

What are the stages of Hypertensive Retinopathy?

A

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
Q

Red EYE Classification?

A

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

Jan Stuff (6 decks)

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