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Year 4 CCC conditions > CKD + Hypertension > Flashcards

CKD + Hypertension Flashcards

1
Q

definition of chronic kidney disease

A

Abnormalities of kidney structure or function present for 3 months with implications for health. Evidence of Kidney disease include the following

1) albumin:creatinine ratio >3mg/mmol
2) eGFR <60ml/min/1.73²

3) evidence of kidney damage, 1 of the following
 albuminuria/proteinuria
 hematuria
 electrolytes abnor due to tubular disorder
 abnor detected by histology
 structural abnor detected by imaging
 hx of kidney transplant

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2
Q

what is the most common cause of CKD

A

DM

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3
Q

aetiology of CKD

A 
DM - most common cause 
HTN - 2nd most common cause 
CV disease 
nephrotoxic drugs 
smoking 
polycystic kidney disease 
glomerular nephrotic and nephritic syndrome
obstructive kidney disease 
atherosclerotic renal vascular disease 
neurogenic bladder 
BPH 
urinary diversion surgery 
urinary stone
schistosomiasis - common in the middle east 
SLE?Vasculitis/myeloma 
amyloidosis
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4
Q

pathophysiology of CKD

A
  • Kidney damage:
  • Proteinuria
  • Haematuria
  • Anatomical abnormality
  • Impaired GFR <60ml/min on at least 2 occasions

leads to
• Fibrosis of tubules, glomeruli and small blood vessels
• Progressive renal scarring
• Mostly irreversible

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5
Q

what are the 2 parameters used in staging CKD

A

GFR

albuminuria

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6
Q

what is the stages of CKD according to GFR criteria

A

stage 1 (normal or high) - > 90

Stage 2 (mildly decreased) - 60-90

stage 3a (mildly to moderately decreased) - 45 - 59

stage 3b (moderately to severely decreased) - 30 - 44

stage 4 (severely decreased) - 15-29

stage 5 (kidney failure) - < 15

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7
Q

what is the stages of CKD according to Albuminuria criteria

A

A1 (normal to mildly inc) - < 3

A2 (moderately inc) - 3-29

A3 (severely increased) - > 30

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8
Q

what are some urine related clinical features of CKD

A
  • Nocturia
  • Polyuria – initial stages due to inability to concentrate urine
  • foamy urine – due to proteinuria
  • hematuria
  • GI symptoms: N+V, anorexia, peptic ulceration (due to urea levels toxic)
  • Pruritus – due to build-up of toxic waste
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9
Q

what are some protein & haemoblobuline related clinical features of CKD

A 
odema 
paller 
lethargy 
SOB 
epistaxis 
brusising - dec erythropoietin production
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10
Q

what are some extra-renal clinical features of CKD

A 
hyperparathyroidism 
bone pain 
osteomalacia 
- dec Ca, inc PO4, incPTH 
peripheral paraesthesia and weakness 
autonomic dysfunction - postural hypotension and disturbed GI motility
depressed cerebral function 
median tunerl compression 
amenorrhea 
erectile dysfunction 
infertility 
restless leg syndrome - due to ureamia build up
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11
Q

how do you diagnose a patient with CKD

A

serum creatinin - for eGFR

  • if < 60, repeat wihtin 2 weeks
  • if no deterioration, repeat within 3 months
  • if still between 45- 59 & no proteinuira (ACR<3), confirm diagnsiss using eGFRcystatinC test

ARC ration & haematuria dip

  • if ACR between 3 and 70, repeat within 3 months with an early mornign urine sample
  • it initial ACR > 70, no need for further testing
  • use urine dip strips to test for haematuria –> investigate further if strips shown 1+ or more blood
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12
Q

who would need a renal USS when diagnosing CKD

A
  • Accelerated progression of CKD - >25% or > 15GFR dec in 1 year
  • Visible or persistent invisible hematuria
  • Symptoms of urinary tract obstruction
  • Fhx of PCKD & are over 20 yrs old
  • GFR < 30
  • Who would need a renal biopsy
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13
Q

who would you refer to renal specialist for further care when diagnosing CKD

A
  • eGFR <30 or a dec of >25%/15ml/min in the last 12 months
  • ACR of >70mg/mmol
  • ACR of >30mg/mmol + persistent haematuria + ruled out UTI
  • Poorly controlled hypertension
  • Rare/genetic cause of kidney disease
  • Suspected renal artery stenosis
  • Renal anaemia
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14
Q

what is the pharmacological treatment of CKD

A

HTN control
- • Off a renin-angiotensin system antagonist to people with CKD and
o DM and ACR >3
o HTN and ACR > 30
o ACR > 70
o Renin-angiotension sytem antagonist  ACEi, ARB, renin blocker (Aliskiren), alderstone antagonist (spironolactone)

• Follow normal HTN guideline for CKD + HTN + ACR < 30

atorvastatin 20mg

aspirin or clopidergrea for secondary preventionm of CKD

apixaban if eGFR 30-50 + non-valvular AF + prior stroke/>75/HTN/DM/symptomatic heart failure

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15
Q

what are the causes of secondary HTN

A

Conn’s adenoma
renovascular disease
phaeochromocytoma

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16
Q

definition of white coat HTN?

A

blood pressure that is unusually raised when measured during consultations with clinicians but return to normal when measured in ‘non-threatening’ suitations

  • difference in measurement by 20/10 mmHG
17
Q

what BP measure is stage 1 HTN

A

clinic BP - > 140/90

ABPM/HBPM - 135/85 average

18
Q

what BP measure is stage 2 HTN

A

clinic - 160/100

ABPM/HBPM - 150/95

19
Q

what BP measure is severe HTN

A

clinic - > systolic 180 or diastolic > 110

20
Q

definition of accelerated HTN

A

clinic BP - > 180 + signs of papilloedema +/- retinohaemorrhage

21
Q

Pathophysiology of HTN

A
  • Blood pressure is dependent on cardiac output and peripheral resistance
  • Cardiac output is determined by stroke volume and heart rate
  • Stroke volume is related to myocardial contractility and size of the vascular compartment
  • Cardiac output is ↑ early in the disease course
  • Then cardiac output ↓ but total peripheral resistance ↑
  • Why this happens is not well understood but there are 3 theories:
  • 1) over-reactive renin-angiotensin system = vasoconstriction and retention of Na and H20
  • 2) Overactive sympathetic nervous system = ↑ stress response
22
Q

Aetiology/RF of HTN?

A
  • Age — blood pressure tends to rise with advancing age.
  • Sex — Up to about 65 years, women tend to have a lower blood pressure than men. Between 65 to 74 years of age, women tend to have a higher blood pressure.
  • Ethnicity — people of Black African and Black Caribbean origin are more likely to be diagnosed with hypertension.
  • Genetic factors — research on twins suggest that up to 40% of variability in blood pressure may be explained by genetic factors.
  • Social deprivation — people from the most deprived areas in England are 30% more likely to have hypertension than those from the least deprived.
  • Lifestyle — smoking, excessive alcohol consumption (recently shown that this has a large influence on BP), excess dietary salt, obesity, and lack of physical activity are associated with hypertension.
  • Anxiety and emotional stress — can raise blood pressure due to increased adrenaline and cortisol levels.
23
Q

how you would you measure BP in clinic

A

1) measure BP in both arms
- if > 15 difference, measure a 2nd time
- if still different, take the higher reading

2) if BP reading > 140/90 during clinic, take a 2nd reading
- if still significantly different, take a 3rd reading and record the lowest 2 reading

24
Q

how you confirm a diagnosis of HTN

A

if clinic reading between 140/90 and 160/110, the offer ABPM or HBPM for confirmation

if clinic reading > 180/120 but no signs of papilloedema and retinal haemorrhage –> repeat BP reading in clinic in 7 days but investigates for end-organ damages

if clinic reading > 180/120 + signs of papilloedema and retinal haemorrhage –> refer to specialist same day

25
Q

what do you do if you suspect phaemochromocytoma

A

refer same day

phaeochromocytoma –> labile or postural hypotension, headache, palpitations, pallor, abdo pain or diaphoresis

26
Q

what tests should you conduct for investigating causes, target organ damage & cardiovascular risk of HTN

A

CVD risk - total cholesterol, HDL, QRISK2

ECG - LVH, cardiac function

urine sample - ACR, haematuria

blood - FBC, U&Es, glucose, HbA1c, ceatinine, eGFR, CKD

examine fundi for end organ damage

27
Q

what should you do if HTN is not diagnosed

A

check BP every 5 years

28
Q

what is the target of control for HTN

A

under 80 yrs old
< 140/90 in clinic

over 80 yrs old
< 150/90 inc clinic

29
Q

management of stage 1 HTN

A

lifestyle management only

if < 80 yrs old with target organ damage, CVD, renal disease, DM, > 10% of QRISK2 scores –> discuss antihypertensive

<60 yrs old with QRISK < 10% –> consider antihypertensive

> 80 with clinic BP >150/90 –> consider antihypertensive

30
Q

management of stage 2 HTN

A

start antihypertensive regards of age

31
Q

what is step 1 of HTN treat ment

A

< 55 and non-black
- ACEi or ARB

> 55 or black
- CCB or thizade diuretics

32
Q

what medications would you give to younger/women of childbearing age?

A

beta-blocker

since ACEi and ARB are contra-indicative to women in pregnancy

33
Q

what is step 2 of HTN treatment

A

ACEi/ARB + CCB/thiazide diuretics

if black - try ARB before ACEi

34
Q

what is step 3 of HTN treatment?

A

ACE/ARB + CCB + Thiazide diuretics

35
Q

what is step 4 of HTN treatment

A

4th antihypertensive +/- specailist advice

  • spironolactone (if K+ < 4.5)
  • alpha or beta blocker (if K+ >4.5)
    in both cases monitor Na, K and renal function within 1 month
36
Q

what are some complictions for HTN

A 
heart failure
coronary artery disease 
stroke 
CKD 
peripheral arterial disease 
vascular dementia
37
Q

what should be discussed in annual review of HTN

A

lifestyle
symptoms
medications - inc side effect
BP - if raised
- check 2-3 occasions over the next few weeks/months
- exclude secondary causes
• Consider additional hypertensives – also applicable if side effects from current medication
• If normal then review in 12 months or consider stopping/reducing antihypertensive

renal function - serumc creatinine, U&Es, eGFR, dipstick for proteinuria

reassess QRISK 2

Year 4 CCC conditions (7 decks)

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