HTN, CKD, HLD Flashcards
Cardiac complications of HTN
CAD Stroke MI vascular / haemorrhagic stroke vascsular dementia
When to suspect HTN
clinic BP reading of 140 / 90 or above
target organ damage
retinopathies
stroke / MI / atherosclerosis / HF / Chronic HD
renal failure (proteinuria)
Causes of secondary HTN
CHAPS
Cushing’s (cortisol ^ > + RAAS - vasodilatory system)
Hyperaldosteronism (^ aldosterone > ^ K+ OUT ^ Na+ IN ^ water retention)
Aortic coarctation (^ myocyte contraction of LV to force blood through aortic narrowing)
Pheochromocytoma (rare aldrenal gland non-cancerous tumor)
Stenosis of renal artery (v GFR > ^ BP to reperfuse kidneys)
+(Pregnancy, COCP, RICP, trauma, white coat syndrome)
Staging cut offs
Pre HTN = 120/80 - 139/89
Stage 1 = 140/90 - 159/99
Stage 2 = 160/100 and above
(Stage 3 = 180/120 and above)
HTN + T2DM treatment first line
ACEi / ARB
HTN w/o T2DM + Black African etc. treatment first line
CCB
HTN w/o T2DM + > 55 y/o treatment first line
CCB
HTN w/o T2DM, not Black African + < 55 y/o treatment first line
ACEi / ARB
HTN + T2DM treatment second line
ACEi / ARB
+
CCB / thiazide - like
HTN w/o T2DM + Black African etc. treatment second line
CCB
+
ACEi / ARB / thiazide - like
HTN w/o T2DM + > 55 y/o treatment second line
CCB
+
ACEi / ARB / thiazide - like
HTN w/o T2DM, not Black African + < 55 y/o treatment second line
ACEi / ARB
+
CCB / thiazide - like
HTN treatment third line
ACEi / ARB \+ CCB \+ thiazide - like
HTN treatment fourth line
- ABPM / HBPM
- consider low dose spironolactone (if K+ < 4.5)
- a X / b X (if K+ > 4.5)
- seek expert advice
HTN in DM treatment principles
lifestyle mod
- T1DM first line = RAAS mod
- T2DM first line = AACEi / ARB
HTN in renal disease treatment principles
if kidney function v = lifestyle mod (ACEi / ARB can be nephrotoxic)
if kidney function - = ACEi / ARB
HTN in pregnancy treatment principles
lifestyle mod
+ specialist referral
+ trial alternative drugs eg. labetalol
+ monitor for pre-eclampsia (urine dip + BP + Sx)
+ arrange for secondary emergency care if pre-eclampsia is suspected
CKD on examination
cognitive impairment
HTN / dehydration
hepatomegaly + bladder distention + BL flank masses
peripheral oedema
‘beer’-like urine
malnutrition
NB. not seen until substantial disease progress
CKD RFs
intrinsic kidney damage - HTN, DM, glomerulonephritis
Nephrotoxic drugs - ACEi, ARBs, bisphosphonates, NSAIDs, ciclosporin
obstructive uropathies
CVD
CKD first line investigations
BTing - ACR, eGFR, U&Es, HbA1c, lipids
EMUS - ACR
urine dip - haematuria / sediment abnormalities
eg. RBC = glomerular disease, WBC = pylenonephritis, Granular casts / renal tubular cells = parenchymal disease
Renal USS - stones, obstruction, PCKD
CKD Management
treat underlying cause monitor disease progression modify lifestyle manage psychological impact CVD risk management
Types of hyperlipidaemia
primary - hereditary
TC can be 7-20 mm/L
statins may not cause much change
secondary
can treat more aggressivelyHLD Management
Primary prevention - atorvastatin 20 mg (if CVD risk and QRISK 10%)
Secondary prevention - atorvastatin 80 mg
