PATHOLOGY -Hypertension

Question 1

what is classified as Hypertension ?

1

Answer 1

1-BP over 140/90

remember there are 3 stages

Question 2

Incidence of Ht ?(1)

Answer 2

1-very very common

for every 10 people diagnosed ,7 are non diagnosed

Question 3

whats primary/secondary HT

2

Answer 3

1) primary = just High Bp ( genetics ,environment etc)

2) secondary = underlying cause to HT, once treated High BP will go away !

Question 4

how do we look for high bp?

(4) main points

Answer 4

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

Question 5

what are the target organs and how can we tell if they’re damaged ?
(4)

Answer 5

1- heart ( LV hypertrophy )
2-Kidney =protein in URINE = leaks protein (creatinine levels high as well )
3-EYE = retinal disease
4-artery walls=atherosclerosis

Question 6

What are the secondary causes of hypertension ?

5

Answer 6

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

Question 7

how can we calculate the risk for the patient ?
(2)
What are the cautions ?
(4)

Answer 7

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 !

Question 8

what lifestyle factors can effect blood pressure ?
(6)
list social factors

Answer 8

1-lifestyle (drugs, alcohol , smoking etc)
2-low income , high income areas
3-family history 
4-other diseases
5-atherosclerosis 
6-drugs and alcohol

Question 9

how can you manage Hypertension ?
(LIFESTYLE )
(6)

Answer 9

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

Question 10

how can we manage Hypertension with drugs ?

6

Answer 10

<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

Question 11

what is FH ?
(5)
familial hypercholesterolaemia

Answer 11

-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)

Question 12

how can you treat FH?

3

Answer 12

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

Question 13

How can you spot lipid disorders?

6

Answer 13

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 )

Question 14

what is Dysbetalipoproteinemia?

3

Answer 14

• mutation of APO-E gene which is autosomal recessive
• causes increase in TRG
• Increase in lipid deposition
• increases premature CV disease

Question 15

what are the other lipid diseases can you name ?
(4)
FTFP

Answer 15

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

Question 16

how can we predict the risk for disease?

2

Answer 16

QRISK3
( uses age, height, weight, lifestyle )
make sure to always use your own professional judgement too )

Question 17

what lifestyle modification can help modify a persons lipid profile ?
(4)

Answer 17

• 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

Question 18

name lipid, cholesterol-lowering drugs, how do they work?
(5)
SPEFC

Answer 18

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)

Question 19

How do statins work ?

4

Answer 19

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

Question 20

define:
ischaemia
infarction 
What factors are they dependent on ? 
(6)

Answer 20

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 )

Question 21

how does atheroma occur and its complications

10

Answer 21

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)

Question 22

what is an abdominal aortic aneurysm (1)
Rupture effects —-(7) just name 3
who is screening available for —
(4)

Answer 22

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

Question 23

what is a dissecting aneurysm

2

Answer 23

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

Question 24

what is a berry aneurysm

Answer 24

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

Question 25

what is a Charcot Bouchard aneurysm ?

Answer 25

-aneurysm of capillaries = micro aneurysm (intracerebraal capillaries )
-can occur due to HT/diabetes
It can cause :
1-rupture which would lead to intercerebral haemorrhage

Question 26

what is vasculitis ?
due to—
complications—-
(8)

Answer 26

-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