PATHOLOGY -Hypertension Flashcards
what is classified as Hypertension ?
1
1-BP over 140/90
remember there are 3 stages
Incidence of Ht ?(1)
1-very very common
for every 10 people diagnosed ,7 are non diagnosed
whats primary/secondary HT
2
1) primary = just High Bp ( genetics ,environment etc)
2) secondary = underlying cause to HT, once treated High BP will go away !
how do we look for high bp?
(4) main points
1-Fundoscopy = white blots , bleeding =>high BP (eye exam)
2) BP in clinic
3) Avoid white coat effect = ambulatory Bp ( done living daily life )
4) check heart , organs
5) check pulse : rate, rhythm ,symmetry,radio -femoral delay
what are the target organs and how can we tell if they’re damaged ?
(4)
1- heart ( LV hypertrophy )
2-Kidney =protein in URINE = leaks protein (creatinine levels high as well )
3-EYE = retinal disease
4-artery walls=atherosclerosis
What are the secondary causes of hypertension ?
5
NUMBER ONE CAUSE IS renal disease
1-Primary hyperaldosteronism =too much aldosterone (increases water retention)
2-Cushings syndrome (too much steroid hormones )
3-renal artery stenosis =narrowing of artery to the kidney
4-coarctation =narrowing of aorta
how can we calculate the risk for the patient ?
(2)
What are the cautions ?
(4)
1- use website = QRISK 3=risk predicting algorithm ( educated guess)
2-looks at all the risk factors and comes up with a risk percentage (ie : 12%)
- doesn’t work if someone has already had cardiovascular event
-only use in primary prevention
-only an APPROXIMATION
-doesnt ask about everything ie : HIV, DRUGS, AUTOIMMUNE DRUGS , TREATMENTS, etc
-dotn use for type 1 diabetes , chronic kidney disease, hypercholesterolemia= already high risk !
what lifestyle factors can effect blood pressure ?
(6)
list social factors
1-lifestyle (drugs, alcohol , smoking etc) 2-low income , high income areas 3-family history 4-other diseases 5-atherosclerosis 6-drugs and alcohol
how can you manage Hypertension ?
(LIFESTYLE )
(6)
1-stop smoking!!! (reduced cardiovascular risk )
2-healthy BMI=20-25 ( body weight)=Exercise
3-healthy diet
4-decreased na+ intake
5-lowered alcohol intake
6-lower caffeine intake
how can we manage Hypertension with drugs ?
6
<55 and white = Ace inhibitors (/ arbs)
>55 and black = ca2+ channel blockers
2)then combine them
3) thiazide like diuretics
other
- Ca2+ channel blockers
- renin inhibitor
what is FH ?
(5)
familial hypercholesterolaemia
-FH = autosomal dominant , causes an increase in LDL in arteries causing blockage of arteries
-there is mutation in the gene which can cause:
-faulty LDL receptor so LDL (mainly cholesterol) isn’t taken into liver cell
-Faulty app B100 which means the receptor won’t recognise it !
-fault is PCSK9 which means that less LDL is taken into the cell =MORE LDL IN BLOOD /Arteries
(you can spot things like a white ring around the eye. achillies tends englargement )
- causes risk of premature cardiovascular disease
-atheroscerosis ( build up of fat in artery walls)
how can you treat FH?
3
1-clincal consultation ( family history , if person had a family member who had MI before age of 60)
2-lipid profile( cholesterol >7.5mmol/L)
3-Genetic screening , can you find the gene mutation in the gene coding for LDL receptor ? use SIMON BROOME CRITERIA to decide who gets a screening
How can you spot lipid disorders?
6
1-CV event 2-Physical signs such as : -xanthelasma ( yellow plaque around eye) -cornea arcus( white ring around eye) -tendon xanthoma=thickening of tendons -eruptive rashes -Lipaemia retinalis( vessels appear white in the back of the eye ) 3)Acute pancreatitis 4)Blood looks abnormal 5)patient chosen for testing 6)FAMILY HISTORY ( very useful for cascade testing )
what is Dysbetalipoproteinemia?
3
- mutation of APO-E gene which is autosomal recessive
- causes increase in TRG
- Increase in lipid deposition
- increases premature CV disease
what are the other lipid diseases can you name ?
(4)
FTFP
1-Familial Chylomicronaemia ( too many chylomicrons in the blood)–>increased TRG
2-Tangier disease=mutation in the gene that codes for HDL, tonsils become full of cholesterol
3-Fish-eye disease=clouds cornea, genetic fault in LCAT (enzyme that is used to convert free cholesterol into the cholesterol ester on high density lipoprotein )
4-Polygenic Hypercholesterolaemia= inherits many genes which make them more susceptible to increased cholesterol
how can we predict the risk for disease?
2
QRISK3
( uses age, height, weight, lifestyle )
make sure to always use your own professional judgement too )
what lifestyle modification can help modify a persons lipid profile ?
(4)
- diets (especially the portfolio diet, cholesterol lowering plan in heart UK)
- reduced fats, sugar, eat wholegrain, plant sterols , fruit veg, fish x2 a week, maintain healthy weight
- reduced alcohol intake
- quit smoking
name lipid, cholesterol-lowering drugs, how do they work?
(5)
SPEFC
Drugs in common use :
1)HMG-CoA reductase inhibitor, so cholesterol can’t be made = STATIN( GI problem, muscle pain BUT well tolerated and very sufficient )
2) Ezetimibe (stops the absorption of cholesterol, well-tolerated BUT can cause GI problems)
3) PCSK-9 inhibitors (receptor is RECYCLED so LDL is taken into the cells more, no side effects, extremely effective BUT very EXPENSIVE )
4) Fibrates =act in the nucleus and cause transcription of genes for lipoprotein lipase,apoA1,apoA5= reduced amount of VLDL and TRG= GI problems, muscle pain
5) Colesevelam–>blocks cholesterol in the gut, stops the absorption ( sticks to other drugs and MAJOR GI disturbance, not well tolerated)
How do statins work ?
4
1-enzyme called HMG-CoA reductase = turns HMG-CoA into mevalanate …. eventually cholesterol
2-this is inhibited so cholesterol levels are reduced
3-cells become starved for cholesterol so they TURN ON LDL receptors , which also reduces circulating LDL
4-Rosuvastatin , Atorvastatin,Simvastatin,Pravastatin
define: ischaemia infarction What factors are they dependent on ? (6)
Ischaemia = lack of blood flow , deprivation of oxygen which can be REVERSED
Infarction = death of tissue as a result of ischaemia = IRREVERSIBLE
dependent on:
1-Nature of blood supply, is there an alternative source ?
2-Rate of development , slow development allows time to find alternative blood flow
3-Vulnerability of tissue to hypoxia =how long can the cells last without oxygen ( neurones = die in 3-4 min and Muscle cells can last many hours)
4-Oxygen content of blood (anemic patients will be more susceptible to Ischaemia )
how does atheroma occur and its complications
10
1-LDL deposits in tunica intima and becomes oxidised by metallo proteases ) Now it cant leave the intima. This causes the endothelial cells to produce receptors for WBC
2-Monocytes bind to receptor and enter the cell = Macrophage
3-Macrophages = bind to Oxidsed LDL = takes in the OxLDL = FOAM CELL
4-FOAM cell =release IGF1 which promotes the migration of smooth muscle cells(SMC) from tunica media –>intima
5-SMC proliferation occurs , this also makes more collagen and the plaque hardens
6-FOAM cells die and release lipid content/DNA material, which is treated as infection so neutrophils are attracted here = inflammation increases
7-THROMBOSIS occurs and a clot forms
COMPLICATIONS :
1-THROMBOSIS ( plaque ruptures)
2-progressive lumen narrowing =ischaemia of organ
3-erosion of tunica media =leads to aneurysm
4-dislodgement of plaque into the blood stream = EMBOLI ( part of plaque floating in blood stream)
what is an abdominal aortic aneurysm (1)
Rupture effects —-(7) just name 3
who is screening available for —
(4)
AAA-most common sort of aneurysm =Abnormal dilation of blood vessels (x>50% of normal )
- CLOT /THROMBUS forms in arteries bellow kidney
- thrombus formation can cause rupture ( if the plaque Is bigger than 5.5cm ) which would lead to :
- thrombus formation =emboli (broken bit of plaque )
- Lilac arteries ( thickened walls, smaller lumen , peripheral vascular disease)
- sudden onset HYPOtension (low BP)
- Pulse in abdominal mass
- Pain in back / flank
- screening is available for men over the age of 65
what is a dissecting aneurysm
2
Blood flows through a tear in the tunica intima into the TUNICA MEDIA decreases blood flow .
1-Blood flows into ADEVENTIA –>PERICARDIUM–>pleural cavity and other structures=HAEMORRHAGE
2-Blood re enters aortic lumen = double barrelled aorta
3-blood may extend down smaller arteries and compress / block them = end organ INFARCTION
what is a berry aneurysm
Berry aneurysm caused by (hypertension,smoking or inherited )
- occurs in circle of willis , where the normal muscular wall is replaced by fibrous tissue –>can lead to SUBARACHNOID HAEMORHAGE ( THUNDER CLAP HEADACHE)
- stiff neck
- fainting
- vomiting
- stroke like symptoms
what is a Charcot Bouchard aneurysm ?
-aneurysm of capillaries = micro aneurysm (intracerebraal capillaries )
-can occur due to HT/diabetes
It can cause :
1-rupture which would lead to intercerebral haemorrhage
what is vasculitis ?
due to—
complications—-
(8)
-inflammation of the vessel wal
-classified by size of the blood vessel it effects
due to :
1-Antigen antibody deposition in the vessel wall
2-Autoimmune diseases: rheumatoid arthritus
3-Henoch Schonlein purpura: disease which involves inflammation of small blood vessels
4-Polyarteritis nodosa: inflammation of medium arteries ie: Hep B infection
COMPLICATIONS : 1-thrombosis 2-ischaemia (claudication type pain in jaw ) 3-Infarction 4-skin rashes and kidney dysfunction
