GP Flashcards
How is HTN diagnosed
140/90 on 2 separate occasions
stage 1 - 140/90
stage 2 - 160/100
severe - 180/110
AMBP - uses average of 14 measurements
Causes/RF of essential and secondary HTN
essestial (no underlying cause)
- low birth weight
- obesity
- XS alcohol
- XS salt
Secondary
- renal disease
- endocrine
- pre-eclampsia
- drugs (OOC, steriods, NSAIDS)
Step 4 of HTN medical management
+further diuretic
OR
+alpha blocker
OR
+beta blocker
Mechanism of action and 1 example of each diuretic type
- thiazide (indapamide) inhibits Na reabsorption and inhibits Na/Cl transporter in DCT
- loop (furosemide) inhibit Na/Cl in ascending limb
- Potassium sparing (triamterene) antagonise actions of aldosterone in DCT, more Na into collecting duct -> excreted. Na reabsorption inhibited so less K and H exchanged and lost in urine - K sparing
- Aldosterone antagonist (spironolactone) helps loop/thiazide but antagonising aldosterone
CCB example and MoA
amlodipine, nifedipine
decrease myocardial contractility, relaxes vascular SM, reduces systemic VR and arterial BP
ACE-I example and MoA
Ramipril
decreases angiotensin II formation so decreased vasocontriction
blocks degradation of bradykinin (vasodilator)
ARB example and MoA
candesartan
block angiotensin II receptors, down regulates sympathetic adrenergic activity, promotes renal excretion Na and H20
dilates vessels reducing arterial pressure, preload and afterload on the heart
B blockers example and MoA
bisoprolol
blocks adrenaline and noradrenaline binders
Describe the link between ED and HTN
30-40% men with HTN also have ED
HTN stops penile arteries dilating and makes SM lose ability to relax (not enough blood to penis to cause erection and blood vessel damage)
Diuretics decrease force of blood to penis and zinc (needed to make testosterone)
BB dampen response to nerve impulses that lead to erection
Effects of angiotensin II on body
IN REPSONSE TO LOW BP (decrease in renal perfusion JGA)
- increased sympathetic activity
- Tubular Na and Cl reabsorption and K excretion
- Aldosterone secretion (adrenal) -> contributes to 2
- arteriolar vasocontriction
- ADH secretion (pit gland) -> H20 absoption CD
Heart failure causes
10% of pt>65
- myocardial dysfunction
- cardiomyopathy
- factors increasing myocardial work (obesity, anaemia)
- HTN
- XS alcohol
Compensatory mechanisms for HF
- Sympathetic NS
- increases HR + SV (faster more forceful contractions)
- less effect after repeated action
- Increased Pre load
- ADH and aldosterone increase filling volume.
- increased Preload, higher pressure, higher SV
- need more 02 that isnt supplied -> muscle death
- Hypertrophy
- heart muscles enlarges to produce stronger contractions but needs more 02 that isnt supplied. Concentric hypertrophy reduces ventricle volume
Heart failure symptoms and signs
*SOB
*ankle swelling
*fatigue
+orthopnoea (SOB when flat)
Signs- peripheral oedema, pul crackles, tachy, increased JVP
Heart Failure diagnosis
- BNP (increased LV dysfunction)
- <100 normal
- 100-400 refer echo 6/52
- >400 refer echo 2/52
- Echo (US waves look at pumping action and structure)
- LVSD - decreased LVEF <40%
- CXR
- Bloods (eGFR normal 90-100%)
CXR findings in Heart failure
Alveolar oedema
B lines
Cardiomegaly
Dilated prominent vessels
Effusion pleural
Medical management of Heart failure
1st - ACE, BB (start low go slow)
2nd - Aldoserone antagonist, ARB (if pt doesnt tolerate ACEI)
Hydralazine and nitrate if pt black
Diuretics relieve symptoms
Heart failure prognosis
30-40% die in first year
<10% mortality following
2/3rd pt die in 5 years
CVD primary, secondary, teritary prevention
1- lifestyle
2- medication, Q risk 2
3- rehab
Polypharmacy issues
Interactions
non adherence
NHS cost
Prescribing cascade
88% chance of adverse drug even if 5+ meds
Notifiable diseases
(6 in 1) Whooping Cough, Tetanus, Diphtheria
(MMR) Measles, Mumps, Rubella
Malaria
meningococcal septicaemia
Scarlet Fever
TB
Acute encephalitis