Cardio

Question 1

STEMI vs NSTEMI

Answer 1

Stemi is transmural infarction

Nstemi is sub endocardial infarction

Question 2

MAP =

Answer 2

Diastolic pressure + 1/3(pulse pressure)

Question 3

Complications of hypotension

Answer 3

Circulatory collapse (vessel collapse)
Tissue ischemia/hypoxia
No filtration in the kidney
MAP below 60 can cause syncope

Question 4

Complications of hypertension

Answer 4

Renal, retinal damage 
Oedema 
MAP above 160 can cause cerebral oedema 
Aneurism/haemorrhage 
Heart hypertrophy/failure

Question 5

What organ influences blood volume ?

Answer 5

Kidney

Question 6

What influences TPR

Answer 6

Vessels

Sympathetic nervous system

Question 7

What influences CO

Answer 7

Vessels

Sympathetic nervous system

Question 8

Where are blood pressure receptors located ?

Answer 8

High pressure baroreceptors in aortic arch (CNX) and carotid bodies (CNIX)
–> vasomotor centre, cardio-inhibitory and -acceleratory centres

Low pressure baroreceptors in venous system and right atrium

Question 9

Decreased sympathetic impulses to heart due to increase BP results in

Answer 9

Decreased HR and contractility –>

Decreased CO

Question 10

Sympathetic nervous system influences blood pressure by:

Immediate changes

Answer 10

Releases NA onto heart to increase CO (positive chronotropic and inotropic effects) (B1 receptors)

Releases NA onto blood vessel smooth muscle to cause constriction or relaxation (overall constriction)
(B2 receptors - vasodilation; a1 receptors - vasoconstriction)

Activated the RAAS (kidney) (NA on a1 receptors)

Question 11

Hormones released by kidney that affect BP

Answer 11

ANP
ADH
RAAS

Question 12

Aldosterone is secreted by… And acts on…

Answer 12

Adrenal cortex zone glomerulosa

Stimulates
Na resorption
Water reabsorption
K and H+ excretion

Question 13

Release of aldosterone is regulated by:

Answer 13

AII
Potassium increase (or decreased na)
ACTH from anterior pituitary
ANP (opposes)

Question 14

What does AII do?

Answer 14

Aldosterone secretion
ADH release by posterior pituitary
Vasoconstriction
Activated SNS

Question 15

ADH is synthesised in the

Answer 15

Hypothalamus

Paraventricular and supraoptic nuclei

Question 16

What does ADH do?

Answer 16

Acts on V1 receptors in kidney - DCT and collecting ducts

Acts on V2 on blood vessels - vasoconstriction

Increased no of aquaporins

Question 17

What causes release of ADH

Answer 17

Change in osmolality (osmoreceptors in hypothalamus) (1-2%)

Fall in blood volume (10%
1-2% change sensitises osmoreceptors)

Question 18

BP =

Answer 18

CO X PR

Question 19

Hypertension means

Answer 19

Diastolic over 90

Systolic over 140

Question 20

Heart hypertrophy is an adaptive response to pressure overload which in turn causes :

Answer 20

Atrial enlargement and fibrillation
Ventricular dilation
Congestive heart failure
Sudden death

Question 21

Gross changes in benign nephrosclerosis

Answer 21

Normal or slightly reduced size
Fine, leathery granular cortical surface
Cortical scarring and shrinking

Question 22

Malignant HTN and accelerated nephrosclerosis , gross changes:

Answer 22

Pinpoint petechial haemorrhages on cortical surface due to rupture of arterioles or glomerular capillaries
“Flea-bitten” appearance

Question 23

Im atherosclerosis collagen is produced by… And degraded by…

Answer 23

Smooth muscle cells
Metalloproteases elaborated by macrophages

Therefore plaques with large numbers of inflammatory cells are more vulnerable to rupture

Question 24

Statins

Answer 24

HMG-CoA reductase inhibitors

Reduce plaque inflammation and increase plaque stability AND cholesterol lowering effect

Question 25

What is a stunned myocardium

Answer 25

Persistent abnormalities in cellular biochem after MI that result in a non contractile state for at least several days, myocardium remains profoundly dysfunctional

Question 26

What are the three patterns of infractions and how do they show up on ECG

Answer 26

Transmural:
ST elevation and loss of Q waves and loss of R wave amplitude

Sub endocardial:
NSTEMI
No Q waves
Region most vulnerable to hypoxia and hypoperfusion

Microscopic:
Almost no ecg changes
Can be due to vasculitis, emboli station of valve vegetarians or mural thromboxane or vessel spasm due to elevated catecholamines (eg stress)

Question 27

Timeline of morphological changes with MI

Answer 27

0-1.5hrs
Relaxation of myofibrils, glycogen loss, mitochondrial swelling

0.5-4hrs
Sarcolemma disruption
Mitochondrial amorphous densities

4-12hrs
Dark mottling on gross 
Ongoing coagulation necrosis 
Pyknosis of nuclei 
Hyper eosinophilic appearance of myocytes 
Beginning neutrophillic infiltrate 
Marginal contraction band necrosis 

1-3days
Mottling with yellow-tan infarct centre
Coagulation necrosis, loss of nuclei and striations, interstitial infiltrate of neutrophils

3-7days
Hyperemic border, central yellow-tan softening
Disintegration of dead myofibers
Dying neutrophils
Early phagocytosis by macrophages at border

7-10days
Depressed red-tan margins
Well developed phagocytosis
Early fibrovascular granulation tissue at margins

10-14 days
Red-grey depressed infarct borders
Well established granulation tissue with new blood vessels and collagen deposition

2-8weeks
Grey-White scar
Increased collagen deposition and decreased cellularity

> 2months
scarring complete or gross
Dense collagenous scar

Question 28

MI

What would peripheral blood biochemistry show?

Answer 28

Troop in T
Creatine kinase (MB)
AST
LD

Question 29

After myocyte injury, tropinin is released

Answer 29

In 2-4 hours and persists for up to 7 days

Troponins can also calculate infarct size but the peak must be measured in the 3rd day

Question 30

CK-MB

Answer 30

Has a short duration and cannot be used for late diagnosis of MI but can be used to suggest infarct extension of levels rise again

Usually back to normal in 2-3days

Question 31

After MI, LDH levels are usually back to normal in

Answer 31

10-14 days

Question 32

Main hostological changes seem in MI pretty early

Answer 32

Loss of striations
Loss of nuclei
Wavy fibers !!!!

Question 33

Sublethal ischemia can also induce

Answer 33

Intracellular myocyte vacuolization

Still viable but frequently poorly contractile

Question 34

Complications of acute MI

Answer 34

Contractile dysfunction 
Papillary muscle dysfunction
Right ventricular infarction 
Myocardial rupture 
(VSD)
Arrhythmias 
Pericarditis 
Chamber dilation 
Mural thrombus 
ventricular aneurysm
Progressive late HF (chronic IHD)

Question 35

Describe the myocardial action potential

Answer 35

Phase 0: rapid depol
Phase 1: partial repol
Phase 2: plateau 
Phase 3: repol 
Phase 4: resting = pacemaker potential

Question 36

The plateau phase on the action potential corresponds to what on the ECG

Answer 36

The ST segment

Question 37

Phase 3 of the action potential corresponds to what on the ecg

Answer 37

T wave

Repol

Question 38

Causes of arrhythmias

Answer 38

Cardiac ischemia
Excessive discharge or sensitivity to autonomic transmitters
Exposure to toxic substances
Unknown

Question 39

Causes of coronary artery occlusion

Answer 39

Atherosclerosis! 
Congenital anomalies 
Coronary artery dissection 
Ostial stenosis 
Coronary arteritis and aneurysms
Traumatic/iatrogenic
Chronic heart transplant rejection 
Spasm (diagnosis of exclusion)

Question 40

Ostial stenosis

Answer 40

Traditionally a feature of syphillitic aortitis
May be isolated
Test for stenosis if you can pass a 2mm probe down it

Question 41

Definition of MI

Answer 41

Increase then fall in tropinin (or CKMB or other) with at least one of following:

• ischemic symptoms
• pathological Q wave on ECG
• ST elevation or depression
• coronary artery intervention eg angioplasty

OR

Pathological changes of acute MI

Question 42

LVH - dyspnea

RVH - ?

Answer 42

Enlarged liver(pain)