Cardivascular

Question 1

Jones major criteria

Answer 1

Migrating Polyarthritis
Pancarditis
Subcutaneous nodules
Sydenhams Chorea
Erythema Marginatum

Question 2

Jones minor criteria

Answer 2

Arthralgia
Fever
Prolonged PR interval
Raised ESR/CRP
Leukocytosis

Question 3

MI time frame, in terms of:
Depletion of ATP
irreversible cell injury
Microvascular injury
Loss of contraction

Answer 3

Depletion of ATP: Starts immediately, 50% gone in 10mins, only 10% left at 40min
irreversible cell injury: 20-40 mins
Microvascular injury: >1hr
Loss of contractility: 1-2 mins (well before myocyte death - due to loss of oxidative metabolism and accumulation of lactate)

Question 4

Serous pericarditis:

Answer 4

Noninfectious inflammatory processes; SLE, RF, Scleroderma, tumours, uraemia, infection in surrounding tissue, e.g. pleural bacterial infection. Mild viral infection elsewhere in the body.

Mild inflammatory infiltrate, lymphocytes. DOES NOT usually organise into fibrous adhesions

Question 5

Fibrous or Serofibrinous pericarditis

Answer 5

Most frequent type of pericarditis.
Mixed serous and fibrinous exudate.
Clinically has a loud pericardial rub.

acute MI
postinfarction syndrome (Dressler sndrome)
uremia
chest radiation
RF
SLE
trauma
cardiac surgery

Question 6

Purulent pericarditis

Answer 6

invasion of pericardial space by microbes
unwell, fever, systemic signs.

Intense inflammatory response and scarring leads to constrictive pericarditis

Question 7

Haemorrhagis Pericarditis

Answer 7

Blood mixed with fibrinous or suppurative effusion.

Often due to tumour invasion of the pericardial space. Also bleeding disorder, following cardiac surgery and TB.

Clinically similar to fibrinous or purulent pericarditis

Question 8

Caseous Pericarditis

Answer 8

TB until proven otherwise
Can also be caused by fungal infection

Frequently causes severe constrictive pericarditis

Question 9

What % of CAD obstruction will cause angina with exercise

Answer 9

75%

Question 10

What % of CAD obstruction will cause angina at rest

Answer 10

90%

Question 11

LAD supplies

Answer 11

apex (both ventricles)
anterior wall LV
anterior 2/3 ventricular septum

Question 12

RCA

Answer 12

R ventricle

post 1/3 septum and posteriobasal wall of LV (in RCA dominant 4/5 people)

Question 13

Circumflex

Answer 13

in RCA dominant, the circum flex only supplies the lateral LV wall (4/5 people)

Question 14

RF pathology

Answer 14

Aschoff bodies
anitschkow cells - macrophages
macCallum plaques - damaged areas from the pressure jets of blood

Question 15

Infective endocarditis

Answer 15

IVDU - right side valves more common, staph aureus
Normal valves - L sided valves, Staph aureus - more virulent!
Damaged valves - usually caused by strep viridans - normal commensuate of the mouth
Prosthetic valves - coagulase negative staph (staph epidermis)

Question 16

adrenoceptors

Answer 16

a1 - vasoconstriction
a2 - mixed, reduction in contractility
b1 - increase heart rate and contractility
b2 smooth muscle relaxation
b3 - lipolysis, relaxtion of detrusor muscle

Question 17

Heart Failure - pressure overload vs volume overload

Answer 17

sarcomeres in parallel vs in series

Question 18

Blood supply to hypertrophied heart

Answer 18

The increase in size is NOT accompanied by an increase in capillary numbers

Question 19

contraction bands

Answer 19

sign of reperfusion injury

Question 20

Libman sacksDisease

Answer 20

Sterile vegitations on mitral and tricuspid valves seen in SLE

Question 21

Dilated Cardiomyopathy

Answer 21

age 20 -50ys
50% mortality 2 years
only 25% survival rate at 5 years
End stage EF <25%

Question 22

DCM causes

Answer 22

20-50% genetic
Non genetic
-myocarditis
-peripartum
-toxic eg EtOH, chemo
-idiopathic

Question 23

High output failure

Answer 23

Hyperthyroidism
Wet beriberi (thiamine deficiency)
Pagets disease of bone (AV fistula)
Large AV fistulas
Gram -ve septic shock
Severe renal or liver failure