1
Q
1) What is CKD (definition used in your notes)?
A
- Long-term abnormal kidney function and/or structure that stays abnormal
- CKD = sustained reduction in GFR and/or urinary abnormalities and/or structural abnormalities of renal tract
- CKD can exist with “okay” GFR early if kidney damage evidence exists (e.g., albuminuria/haematuria)
2
Q
2) What is end-stage kidney failure (kidney failure) definition?
A
- GFR < 15 mL/min/1.73m²
- Or on dialysis / kidney replacement therapy
3
Q
3) What is AKI (definition + clinical detection)?
A
- Sudden decline in kidney function affecting:
- Fluid balance
- Electrolytes
- Acid–base balance
- Detected clinically by:
- Rising creatinine
- Falling urine output
- Early identification + treating the cause quickly reduces complications, damage, and mortality
4
Q
4) CKD epidemiology facts (from notes):
A
- 4th leading global cause of death among non-communicable diseases
- Global prevalence ~9.1%
- More common in females
- Men more likely to progress to kidney failure
- Increases with age
- Higher rates in high-income countries (ageing + better detection/reporting)
- Social deprivation linked to higher prevalence
5
Q
5) CKD causes (UK emphasis):
A
- Leading causes: diabetes, hypertension
- Other causes: renovascular disease, inherited renal diseases, glomerulonephritis, reflux nephropathy, heart failure (cardio-renal), ageing
6
Q
6) CKD “silent but misleading” + symptoms:
A
- Often missed early; symptoms are non-specific
- Fatigue, pain, breathlessness
- Nocturia, polyuria, haematuria
- Weight loss, poor appetite
- Muscle cramps, nausea/vomiting
- Oedema (ankles/feet/hands)
- Itchy skin, restless legs
- Anaemia-type symptoms, insomnia
- Amenorrhoea, erectile dysfunction
- Psychological symptoms/mental health disorders
7
Q
7) Why early CKD diagnosis matters:
A
- Slow/prevent progression to renal failure
- Time to prepare for dialysis/transplant
- Earlier management of complications (anaemia, potassium, BP, Ca/PO₄)
- Better medicines management (dose + side effects)
- CKD = increased CV risk → early diagnosis reduces CV risk
- Timely referral reduces morbidity, mortality, and cost
8
Q
8) Biggest burden of CKD:
A
- Most people do not progress to kidney failure
- Biggest burden = increased cardiovascular disease risk
- Risk rises with:
- Lower eGFR
- Higher ACR
9
Q
9) What does albuminuria/proteinuria indicate?
A
- Indicates kidney damage
- Predicts CKD progression and cardiovascular events
- Proteinuria itself is nephrotoxic (damages renal tubular cells)
10
Q
10) Albuminuria vs haematuria:
A
- Albuminuria usually originates from kidney
- Haematuria may originate from kidney OR urinary tract
11
Q
11) Measurement of proteinuria and thresholds:
A
- Use ACR (albumin-to-creatinine ratio)
- Proteinuria: ACR ≥ 3 mg/mmol
- PCR × 0.7 ≈ ACR
- Albuminuria may be earliest sign of kidney disease
- Used for risk stratification, monitoring, ACEi/ARB/SGLT2 eligibility, and referral decisions
12
Q
12) Visible haematuria management:
A
- Fast-track urology referral
- Imaging and cystoscopy
- Exclude acute renal disease if indicated
13
Q
13) Non-visible haematuria management:
A
- Dipstick 1+ or more
- Confirm on 2 of 3 tests
- Check renal function + proteinuria
- > 60 years → refer urology
- <60 or negative urology → manage CKD or refer nephrology if abnormal
14
Q
14) CKD diagnosis rule:
A
- Abnormalities must persist ≥3 months
- Either markers of kidney damage OR eGFR <60 on two tests ≥90 days apart
15
Q
15) Markers of kidney damage:
A
- ACR ≥3 mg/mmol
- Urine sediment abnormalities
- Persistent unexplained haematuria
- Electrolyte abnormalities due to tubular disorders
- Histological abnormalities
- Structural abnormalities (e.g., polycystic kidney)
- Kidney transplant history
16
Q
16) CKD stages (GFR based):
A
- Stage 1: ≥90 with kidney damage
- Stage 2: 60–89 with damage
- Stage 3: 30–59
- Stage 4: 15–29
- Stage 5: <15 or dialysis
17
Q
17) eGFR categories (G stages):
A
- G1 ≥90
- G2 60–89
- G3a 45–59
- G3b 30–44
- G4 15–29
- G5 <15
18
Q
18) Albuminuria categories (A stages):
A
- A1 <3 mg/mmol
- A2 3–30 mg/mmol
- A3 >30 mg/mmol
19
Q
19) NICE proteinuria management (diabetes):
A
- ACR <3 → monitor annually
- ACR ≥3 → start ACEi or ARB
- Type 2 diabetes + ACR ≥30 → offer SGLT2 inhibitor
- ACR 3–30 → consider SGLT2 inhibitor
20
Q
20) NICE proteinuria management (no diabetes):
A
- ACR <30 → monitor or treat hypertension
- ACR 30–70 → ACEi/ARB if hypertensive
- ACR ≥70 → ACEi/ARB + refer specialist
21
Q
21) Why BP control matters in CKD:
A
- High BP damages glomeruli
- Accelerates CKD progression
- Increases cardiovascular risk
22
Q
22) ACE inhibitors / ARBs benefits:
A
- Reduce glomerular pressure
- Reduce proteinuria
- Slow CKD progression
- Protect cardiovascular system
23
Q
23) BP targets in CKD:
A
- ACR <70 → <140/90
- ACR ≥70 → <130/80
- ≥80 years with T1DM → <150/90
24
Q
24) Resistant hypertension definition:
A
- BP uncontrolled despite 4 antihypertensive drugs
25
25) Salt restriction in CKD:
- Improves BP control
- Reduces fluid retention
- Slows CKD progression
26
26) ACEi/ARB indications for proteinuria:
- Non-diabetic: ACR ≥70 OR ≥30 with hypertension
- Diabetic: ACR ≥3
27
27) ACEi/ARB cautions:
- Potassium >5 mmol/L
- Renovascular disease
- Previous deterioration in renal function
28
28) ACEi/ARB monitoring:
- Check creatinine and potassium before starting
- Repeat 1–2 weeks after initiation or dose change
29
29) ACEi/ARB renal function change rules:
- Accept small creatinine rise
- If creatinine ↑ >30% or eGFR ↓ >25% → investigate/consider stopping
30
30) ACEi/ARB hyperkalaemia management bands:
- K 5.5–5.9 → diet restriction, diuretics, bicarbonate, binders
- K 6.0–6.4 → repeat test, remove drugs, adjust treatment
31
31) ACEi + ARB combination rule:
- Should NOT be used
- ↑ hyperkalaemia and AKI risk
32
32) ACEi principle in CKD:
- Often continued until dialysis required
33
33) SGLT2 inhibitors examples:
- Empagliflozin
- Dapagliflozin
34
34) SGLT2 inhibitors mechanism:
- Block SGLT2 in proximal tubule
- Cause glucosuria + osmotic diuresis
- Reduce intraglomerular pressure
35
35) SGLT2 inhibitors benefits:
- Slow CKD progression
- Reduce cardiovascular risk
- Reduce HF hospitalisation
- Benefits remain until eGFR ~15
36
36) Finerenone class and mechanism:
- Non-steroidal mineralocorticoid receptor antagonist
- Reduces inflammation and fibrosis
37
37) Finerenone indication:
- CKD stage 3–4 with albuminuria in type 2 diabetes
38
38) Cardiovascular risk in CKD:
- CKD increases cardiovascular risk even with mild disease
39
39) Lifestyle measures for CV risk reduction:
- Smoking cessation
- Weight loss
- Exercise
- Salt restriction
40
40) Statin therapy in CKD:
- Atorvastatin 20 mg daily
- Increase if non-HDL reduction <40% and eGFR >30
41
41) CKD anaemia cause:
- Reduced erythropoietin production
42
42) CKD anaemia treatment:
- Iron supplementation
- Erythropoiesis-stimulating agents
43
43) CKD mineral bone disorder:
- Occurs in CKD stage G4–G5
44
44) Mineral bone disorder disturbances:
- Hyperphosphataemia
- Hypocalcaemia
- Secondary hyperparathyroidism
45
45) Treatment for mineral bone disorder:
- Phosphate binders
- Active vitamin D
46
46) AKI causes:
- Pre-renal
- Intrinsic
- Post-renal
47
47) AKI detection criteria:
- Creatinine rise ≥26 µmol/L in 48h
- ≥1.5× baseline in 7 days
- Urine output <0.5 mL/kg/h >6h
48
48) KDIGO AKI staging:
- Stage 1, 2, 3 based on creatinine rise and urine output
49
49) RIFLE criteria:
- Risk
- Injury
- Failure
- Loss
- End-stage
50
50) AKI management STOP:
- Sepsis
- Toxins
- Optimise
- Prescribing
51
51) AKI review ROUNDUP:
- Repeat U+Es
- Obstruction
- Urinalysis
- NEWS
- Dry or wet
- Urine output
- Prescriptions
52
52) Medication review groups in AKI:
- Drugs affecting renal blood flow
- Renally excreted drugs
- Direct nephrotoxins
- Drugs with side effects in AKI
53
53) Drug-induced renal failure categories:
- Pre-renal
- Direct toxicity
- Immunological
- Post-renal obstruction
54
54) Urinalysis diagnostic clues:
- RBC/protein → glomerular disease
- WBC → tubular/interstitial damage
- Uric acid crystals → uric acid nephropathy
55
55) Fluid retention management:
- Fluid restriction
- Low salt diet
- Loop diuretics effective at low GFR
56
56) Hyperkalaemia emergency management:
- ECG if K ≥6
- IV calcium stabilises heart
- Insulin + glucose and salbutamol shift K intracellularly
- Remove K with diuretics/binders
- Dialysis if refractory
PY511
flashcards
Decks in class (29)
# Cards
-
Intro to Hypertension50
-
Treatment of hypertension55
-
Hypertension management38
-
Hypertension just meds43
-
Particle size analysis final49
-
Capsules final50
-
Intro to tableting final45
-
particle science final52
-
Mixing granulation final59
-
Manufacturing final63
-
IHD patho final63
-
IHD lipids final69
-
IHD hyperlipidaemia treatment final52
-
IHD treatment final49
-
IHD hyperlipideamia overview50
-
Renal intro45
-
Measuring renal function42
-
Renal drugs52
-
Uti's52
-
Renal LUT physiology52
-
CKD AKI56
-
Hepatic intro53
-
Hepatic lecc 252
-
Hepatic ADME68
-
Hepatic 5+656
-
Liver pathophysiology60
-
Cirrhosis complications49
-
Liver blood tests30
-
Discharge35
