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)