Week 9: Hypertension, CKD, hyperlipidaemia Flashcards
(40 cards)
1
Q
stage 1 hypertension
A
>140/90 mmHg
2
Q
stage 2 hypertension
A
>160/100mmHg
3
Q
stage 3 hypertension
A
>180mmHg or diastolic above 120mmHg
4
Q
main types of hypertesnion
A
essential and secondaey
5
Q
causes and RF for HTN
A
- Essential hypertension (primary cause unknown) accounts for the majority of cases
- Secondary hypertension e.g. causes by renal disease, endocrine disease (cushings), pre-eclampsia, drugs
-
Risk factors
- Excess weight
- High salt intake
- Lack of physical activity
- Stress
- Older age
- Fx
- gender
6
Q
presentation of HTN
A
- Usually asymptomatic (except accelerated (malignant) hypertension)
- Look for end organ damage
- Stroke/TIA
- Dementia
- LVH
- CHD
- PAD
- retinopathy
7
Q
screening for HTN
A
- All adults should have their BP measured at least every 5 years up to the age of 80 and annually there after
- Diagnosis of hypertension is confirmed if a person has:
- A clinic blood pressure of 140/90 mm Hg or higher; and
- ABPM daytime average or HBPM average of 135/85 mm Hg or higher.
- Target organ damage screening: hypertensive retinopathy, left ventricular hypertrophy, blood tests, urinalysis for albuminuria, proteinuria and haematuria
8
Q
unvestigations if HTN
A
- Urine dipstick test for protein and blood
- serum creatinine and electrolytes and eGFR
- renal ultrasound
- 12 lead ECG
- Echocardiography
- Fasting blood glucose
- Cholesterol
9
Q
inevstigations if secondary causes of HTN suyspected
A
- 24hour urinary metanephrines
- urinary free cortisol/dexamethasone suppression test
- renin/aldosterone levels
- plasma calcium
- MRI of renal arteries
10
Q
hypertensive cris’ involve
A
malignant hypertension
hypertensive urgency
11
Q
Malignant hypertension
A
- Systolic >200 mmHg, diastolic >130mmHg
- End organ damage e.g. encephalopathy, dissection, nephropathy, papilledema
- Need same day treatment to reduce bP within minutes to hours
12
Q
Hypertensive urgency
A
>180mmHg without end organ damage- should be treated over next few day and BP repeated within 7 days
13
Q
first line maangement of hypertension
A
-
Lifestyle
- Weight reduction through diet and exercise
- Stopping smoking
- Reduce salt
- then medication added on if doesnt work (or above a certain level)
14
Q
Step 1: if patient is <55 and non-black
A
(A)
- ACEi or ARB
- choose ARB if ACEi causes dry cough)
- do not combine ACEi with ARB
15
Q
Step 1: if patient is >55
A
(C) or (D)
- CCB
- Thiazide like diuretic if CCB not suitable
16
Q
Step 1: if patient is black african or caribbean
A
(C) or (D)
- CCB
- Diuretic if CCB not tolerated
17
Q
Step 1: pt with evidenc eof HF
A
(D)
- thiazide-like diuretic e.g. idnapmide
18
Q
which antihypertensive should not be use din conjunction with diabetes
A
CCB
ACE inhibitors and ARBs are preferred agents in the management of patients with hypertension and diabetes
19
Q
Step 2 choices for hypertension
A
check person is compliant with step 1
-
if initially started on:
- ACEi or ARB + CCB or D
- CCB or D + ACEi or ARB
20
Q
which antihypertensive should not be used in black people
A
ACEi
ARB is preffered
21
Q
step 3 choices for hypertension
A
use ACEi or ARB and a CCB and thiazide like diuretic
22
Q
step 4 choices for hypertension
A
- reistant hypertension
- discuss adherence
- add 4th antihypertensive
- consider referral
- consider further diuretic with low dose spironolactone
23
Q
Chronic kidney disease
Classification
A
Kidney function should be assessed using a combination of GFR and albumin:creatinine ratio (ACR) categories.
- Increased ACR and decreased GFR are associated with increased risk of adverse outcomes.
- Increased ACR and decreased GFR in combination multiply the risk of adverse outcomes.
24
Q
causes of CKD
A
- Diabetes
- Hypertension
- Glomerular disease
- Acute kidney injury
- Nephrotoxic drugs e.g. ACEi, ARB, NSAIDS
- Myeloma]family history
- Obesity
- Gout
25
presentation of CKD
* Symptoms (severe)
* Anorexia
* Nausea
* Fatigue
* Weakness
* Pruritus’
* Peripheral oedema
* Dyspnoea
* Insomnia
* Nocturia/polyuria
* Signs
* Hypertension
* Excoriation
* Pallor
* Peripheral oedema
26
screening for CKD
monitor GFR annually
27
investigations for CKD
* Blood pressure
* Urine analysis
* Protein in urine?
* Blood tests
* Urea and electrolytes
* eGFR
* Bone biochemistry
* Liver function tests (albumin)
* Full blood count
* CRP
* +/- iron levels (ferritin, iron, reticulocyte haemoglobin)
* +/- PTH
28
further investigations for CKD
* Auto-antibody screen (auto-immune)
* Ultrasound
* Kidney size
* Evidence of obstruction (hydronephrosis)
* Kidney biopsy
* Cause unknown
* Haematuria
* Proteinuria
* More specific investigations- CT (stones/mass), MRI (mass), MR angiogram
29
management of CKD is outpatient based
* treat underlying disease
* reduce CVD risk
* reduce progression of CKD
* prevent or treat complications of CKD
30
treating underlying disease in CKD
* Treat and monitor diabetic control
* Treat hypertension
* Treat infections promptly
* Tolvaptan if meets criteria for ADPKD
* Immunosuppression for GN if appropriate
31
reducing CVD risk in CKD
* Start on statin
* Control BP
* Improve control of diabetes
* Advise weight loss
* Advise exercise
* STOP SMOKING
32
reducing progression of CKD
* Reduce proteinuria – ACEi/ARB
* Monitor blood tests
* Control BP
33
prevent or treat complications of CKD
* Dietary advice regarding low phosphate/low potassium diet
* Phosphate binders
* IV Iron/Folate/Vit B12 replacement
* EPO (Erythropoesis stimulating agent)
* Replace Vitamin D deficiency
* Consider Calcimimetics for tertiary hyperparathyroidism
* Dietician input
34
hyperlipidaemia
* Rised serum levels of one or more of total cholesterol (TChol), low-density lipoprotein cholesterol (LDL-C), triglycerides (TGs), or both TChol and TG (combined hyperlipidaemia).
* Dyslipidaemia is a wider term that also includes low levels of high-density lipoprotein cholesterol (HDL-C). Many types of hyperlipidaemia carry an increased risk of cardiovascular disease (CVD).
35
cholesterol should be
\<5
36
causes of hyperlipidaemia
* Poor diet (eating too much saturated or trans fat), obesity, lack of exercise, smoking, alcohol and increasing age.
* Familial hypercholesterolaemia is an inherited autosomal dominant condition. This should be suspected in adults with a total cholesterol level greater than than 7.5mmol/L and/or a personal or family history of premature coronary heart disease, an event before 60 years in an index person or first degree relative.
37
presentation of hyperlipidaemia
* No symptoms
* Signs: corneal arcus, Xanthelasma
38
investigations for hyperlipidaemia
* Lipid profile
* FBG
* Renal function
* LFTS
* TSH
* Do QRiskScore
39
**Management of hyperlipidaemia– aim to prevent CVD**
* Lifestyle changes
* First line: statins (atorvastatin, simvastatin)- inhibit HMG-CoA reductase
* Most effective drugs (aim of \<40% reduction after 3 months)
* issue with myalgia (test for CK)
* Adjuvants/ if statins not tolerated
* Ezetimibe
* Fibrates
* Omega- 3 fish oils
40
MOA or ezetimibe
inhibits the absorption of cholesterol from the [small intestine](https://en.wikipedia.org/wiki/Small_intestine) (NPC1L1 inhibitor) and decreases the amount of cholesterol normally available to liver cells.
The lower levels of cholesterol in the liver cells leads them to absorb more cholesterol from circulation and thus lowering the levels of circulating cholesterol.
