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M201 > W2 CVS > Flashcards

W2 CVS Flashcards

1-23 is blood pressure control molecular basis

1
Q

What is blood pressure? (arterial)

A
  • Pressure exerted on the walls of blood vessels (largely referred to as arterial pressure)
  • Pressure is essential to perfuse all the cells of the entire body (constant & consistent)
  • Measured as systolic/diastolic mmHg
  • BP varies with age and pathological conditions

Systolic BP: MAP during heart contraction
Diastolic BP: MAP during heart relaxation
(Systemic: 120/80 mmHg; Pulmonary: 25/8 mmHg, Venous: 6-8 mmHg)

MAP= Mean arterial pressure

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2
Q

What is the blood pressure calculation?

A

BP= Cardiac output x Peripheral Resistance

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3
Q

What is the Cardiac Output calculation?

A

Cardiac output = Heart Rate x Stroke volume
= 70/min x 70 ml
= 4900 ml/min = 5L/min

CO- how much blood the heart pumps out

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4
Q

If artery size is larger…
If artery size is smaller…

A

….BP is lower
…BP is higher

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5
Q

What is blood pressure?

A
  • Pressure exerted on the walls of blood vessel (largely referred to as arterial pressure)
  • Pressure is essential to perfuse all the cells of the entire body (constant & consistent)
  • Measured in mmHg
  • BP varies with age and pathological conditions
    Systolic BP: MAP during heart contraction
    Diastolic BP: MAP during heart relaxation
    (Systemic: 120/80 mmHg; Pulmonary: 25/8 mmHg, Venous: 6-8 mmHg)
    Blood pressure
    Factors:
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6
Q

What is the calculation for blood pressure?

What is the cardiac output equation?

A

BP= CO X PR

blood pressure= cardiac output x peripheral resistance

Cardiac output= Heart Rate x Stroke Volume
= 70/min x 70mL
= 4900 ml/min = 5L/min

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7
Q

Autoregulation process:
What is autoregulation?
What do changes in blood flow lead to?

A

Normal resting conditions redistribute blood as needed by tissues.
Body wants to maintain normotension

Change in blood pressure leads to Vasodilatation- dec BP (when hypertension) and Vasoconstriction- inc BP (when hypotension)

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8
Q

Autoregulation of perfusion:
When organ/body tissue has low O2 what occurs?

A
  1. CO2 , potassium (K+) or hydrogen (H+) ions
    (acidic pH)
    Lactic acid
    (by-products of cell metabolism)
    Histamine (Inflammation)
    Body temp
  2. Stimulates endothelial cells to release endothelin (peptides)
    Platelet secretions and prostaglandins
  3. Vasoconstriction of pre-capillary sphincters
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9
Q

Autoregulation of perfusion:
When organ/body tissue has High O2:

What takes place?

A

CO2 , potassium (K+) or
hydrogen (H+) ions (acidic pH)
Lactic acid
(by-products of cell metabolism)
Histamine (Inflammation)
Body temp
tissues

Stimulate endothelial cells to release NO (nitric oxide)
Vasodilation of precapillary

Myogenic response
Stretching of the smooth muscle in the
walls of arterioles
Blood flow (High): Stretch
Blood flow (low): Constrict
Localised protective function to maintain
the blood flow:
Ischemia (hypoxia) Vs Excessive perfusion

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10
Q

What is Neural regulation?

A

Short-term regulation of blood pressure, especially in responses to transient changes in arterial pressure, via baroreflex mechanisms

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11
Q

Neural Regulation of LOW Blood pressure
(hypotension)

A

Baroreceptors sense low BP and reduce firing rates (so vagus nerve is inhibited)

CVC in brain stem:
1. Reduce vagal activity
2. CVC inc Sympathetic cardiac activity (to inc HR)
Heart contraction and HR inc
Cardiac Output inc
Blood pressure raises and homeostasis restored

(vagal activity suppresses hr so we want to stop that to inc hr)

Opposite for hypertension occurs

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12
Q

RAAS:
How is Low BP regulated by hormonal regulation?

A

Sensed by kidney. Renal hypoperfusion. Granular cells (juxtaglomerular) stimulate production of/ release of hormone Renin.

Liver synthesises Angiotensinogen. Converted into Angiotensin l and ll by ACE
Lungs- Angiotensin converting enzyme (ACE) is created.
Angiotensin ll stimulates aldosterone release which inc peripheral resistance which inc BP

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13
Q

Hormonal: Erythropoietin (EPO) action when there is low blood pressure:

A
  1. Kidney becomes hypoxic (renal arterial
    oxygen drops) triggering EPO release
  2. EPO stimulate the red bone marrow to
    produce more erythrocytes (RBC)
  3. Erythrocytes increase O2 transport and
    restore O2 level

Too much EPO is a risk:
EPO is a vasoconstrictor.

Increase
Blood viscosity, resistance, and
pressure
Decrease
Blood flow

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14
Q

Catecholamines: Adrenaline/Nor-adrenaline effects on low BP

A
  • Released by the adrenal medulla
  • Enhance and extend the body’s sympathetic activity (“fight-or-flight” response)

Increases:
Heart rate
Force of contraction
Vasoconstriction (non-essential organs)
Energy mobilisation to the liver, muscle and heart
“Fight or Flight”

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15
Q

Sympathetic Vs Parasympathetic activity?

A

Voluntary Vs Involuntary
Fight or Flight Vs Rest and Digest

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16
Q

Hormonal: Antidiuretic Hormone (ADH)/ Arginine Vasopressin (AVP)

When there is Low BP:

A

Hypovolemia: Increase in tissue fluid osmolarity (loss of blood volume) triggers ADH release

  • ADH is secreted by the cells in the
    hypothalamus, transported to the posterior
    pituitary and stored until nervous stimuli.
  • ADH signals kidneys to reabsorb more water
  • Prevent the loss of fluids in the urine.
  • Increase overall fluid levels
  • ADH constricts peripheral vessels.
  • Restore blood volume and pressure.
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17
Q

What are some causes of Hypovolemia? (5)

A

Haemorrhage
Dehydration
Diarrhoea
Burns
Diuretics

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18
Q

What are some causes of Structural dysfunctions? (leading to low HR) (5)

A

Valves disease- valves dont open/close fully
Ischemia- blood flow and thus oxygen is restricted
Myopathy- disease that affects the muscles that control voluntary movement in the body.
Pulmonary hypertension
Pericardial disease

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19
Q

Regulation of Blood pressure control
Includes:

A
  • Autoregulation
  • Changes in blood flow detected by the local receptors during micro perfusion
  • Neural
    Short-term regulation of blood pressure, especially in responses to transient changes in arterial pressure, via baroreflex mechanisms
  • Hormonal
    Long-term regulation of blood pressure
  • Renin-Angiotensin-Aldosterone
  • Anti-diuretic hormone (ADH; arginine vasopressin)
  • Atrial natriuretic hormone/peptide/factor
  • Erythropoietin
  • Adrenaline/Noradrenaline
20
Q

Neural Regulation of HIGH Blood pressure

A

Baroreceptors firing rates inc
Vagal activity inc (which suppresses HR-we want this)
Parasympathetic activity inc
Sympathetic activity dec
HR dec
Heart contraction dec
CO dec
Blood pressure dec and homeostasis restored

21
Q

RAAS high BP

A

Juxtaglomerular cells (granular cells) sense high BP in kidney
JG cells are suppressed so no Renin is released
No Angiotensin l secreted to be converted by ACE into Angiotensin ll and thus no stimulus for Aldosterone release from Adrenal cortex

22
Q

Atrial Natriuretic Peptide (ANP)
Where is it synthesised and released?
What is its function?

A

Synthesised and Released by Atria
Inc sodium in urine

23
Q

What are the risks of Hypertension? (8)

A
  • heart disease
  • heart attacks
  • strokes
  • heart failure
  • peripheral arterial disease
  • aortic aneurysms
  • kidney disease
  • vascular dementia
24
Q

Side effects of antihypertensives:

A

ACE inhibitor- Dry cough
Beta-blocker- bradycardia
Calcium channel blocker- Ankle swelling, flushing palpitations
ARB- Dizziness, headache, fatigue,

25
Q

Name some HMG-coA reductase inhibitors (Statins):

A

Atorvastatin
Simvastatin
Rosuvasatin
Pravastatin

26
Q

Medicines for hypocholesterolaemia:

A
  • Ezetimibe
  • Bempedoic acid
  • Inclisiran (subpopulation of patients in Wales)

specialist care:
alirocumab
evolocumab
volanesorsen

27
Q

What can influence drug distribution in the body?

A

Body weight

28
Q

Which enzyme system is responsible for the metabolism of many antihypertensive drugs?

A

Cytochrome P450 (or CYP450)

29
Q

How can grapefruit juice affect the pharmacokinetics of antihypertensive drugs?

A

It inhibits drug metabolism

30
Q

Which class of drugs can potentially decrease the effectiveness of antihypertensive drugs?

A

NSAIDs

31
Q

How can diuretics interact with antihypertensive drugs?

A

they can enhance antihypertensive effects

32
Q

Angiotensin II Receptor Blockers (ARBs)

A
  • ARBs are receptor antagonists that
    block type 1 angiotensin II (AT1) receptors on blood vessels and other tissues such as the heart.
  • AT1 receptors are coupled to the Gq-protein
    and IP3 signal transduction pathway that
    stimulates vascular smooth muscle
    contraction

The outcome/effect is similar to ACEi’s

33
Q

ARB drugs are usually classed by name such as…

A

‘sartan’ drugs

Candesartan (prodrug)
irbesartan
Losartan (prodrug)
valsartan
olmesartan

34
Q
A

Dihydropyridines more vascular smooth muscle target
Non- Cause cardiac muscle inhibition at the heart.

35
Q

What is the target of thiazide/ thiazide-like diuretics?

A

Sodium, chloride symporters in the DCT, to cause diuresis and excrete sodium
retain it in the urine and not reabsorbed.

36
Q

What are the side effects of Thiazides and Thiazide-like diuretics?

A

*Hypokalaemia (Potassium loss due to increased sodium delivery to distal
tubule)- would expect opp effect but JG cells sense drop in sodium and this causes more sodium/potassium to be pumped in

*metabolic alkalosis (increased hydrogen ion loss in the urine)
*dehydration (hypovolemia),
*leading to hypotension
*hyponatremia

37
Q

Beta-adrenergic receptor antagonist

A

Increases heart rate
Increasing cardiac muscle’s force of contraction
Adrenergic receptor ‘beta’ (B-1)

38
Q

ACE Inhibitors:
How do they work?
(pharmaceutical def)

A

Block synthesis of Angiotensin II by inhibiting ACE (Enzyme Inhibitors)

  1. Ionic bond
  2. Interaction with the labile peptide bond
  3. Additional binding
  4. H-bond
39
Q

Enalaprilat and Enalapril:

A

Carboxylic acid changed to Ester (EWG) so pKa of N has become less basic so wont be protonated, wont become zwitterion so can easily be absorbed

Enapril is a prodrug of Enaprilat

40
Q

What drugs have the same general formula, similar to enalapril? (ACEi)

A

Lisinopril, Ramipril, Quinapril

41
Q

Structure-Activity Relationship of ACEi

A
  1. N-ring must contain COOH to mimic the C-terminal COOH of Angiotensin I
    B. Large hydrophobic heterocyclic rings (i.e., the N-ring) increase potency/PK
    C. Zinc binding groups: SH (Captopril), COOH (Ramipril), or POOH (Fosinopril).
    SH group shows superior binding to zinc but skin rash and taste→
    disturbances
    D. Mimic the Phe. Mimic the peptide hydrolysis transition state. Compensates for
    lack of a SH
    E. Esterification of COOH or POOH produces an orally bioavailable prodrug
    F. X is usually methyl
    G. Stereochemistry needs to be consistent with L-amino acids (natural
42
Q

SAR of 1,4-dihydropyridine

A

A. 1,4-dihydropyridine ring: essential
B. Substituted phenyl ring at C4: optimise activity
C. Substituent X: need to be in ortho or meta. Lock active conformation essential for the activity
D. Ester groups at the C3 and C5 positions optimise activity.
Other EWG: decreased antagonist activity. May have agonist activity
E. If esters at C3 and C5 are non-identical: C4 is chiral→stereoselectivity between the enantiomers is observed (selectivity for specific blood vessels). Marked as racemic
F. All (except amlodipine) have C2 and C6 = CH3.

Enhanced potency of amlodipine : 1,4-DHP receptor can tolerate larger substituents at this position and that enhanced activity can be obtained

43
Q

1,4-dihydropyridine; more info

A

Coadministration of 1,4-DHPs with grapefruit juice: increase the systemic concentration of the 1,4-DHPs. Due to inhibition of intestinal CYP450 by flavonoids and furanocoumarins specifically found in grapefruit juice
- do not drink grapefruit juice whilst taking this drug
Compound ending in -PIDINE

44
Q

Diuretics

A

Increase the rate of urine formation targeting the kidney
Increased excretion of electrolytes (especially Na+ and Cl-) and water without
affecting protein, vitamin, glucose, or amino acid reabsorption
Treatment of oedema (excessive extracellular fluid) (e.g., congestive heart
failure) and in the management of hypertension
Classified by * chemical class (thiazides and thiazides-like)
* mechanism of action (carbonic anhydrase inhibitors and osmotic)
* site of action (loop diuretics)
* effects on urine contents (potassium-sparing diuretics)
Different efficacy (ability to increase the rate of urine formation, e.g increase
the excretion of Na+ filtered at the glomerulus ) and different site of action
within the nephron
🧬💊❤️

45
Q

Thiazide-like Diuretics:
How do they work?
Example?

A

Acting on distal convoluted tubule: compete for Cl- binding site of the Na+/ Cl– symporter inhibiting reabsorption of Na+ and Cl-

Indapamide

Rapidly and completely absorbed from GI. Duration of action of up to 8 weeks.
Extensive binding to carbonic anhydrase in the erythrocytes

46
Q

Anticoagualant Vs Antiplatelet?
What is the difference?

A

Anticoagulants slow down clotting thereby reducing fibrin formation and preventing clots from forming and growing. Antiplatelet agents prevent platelets from clumping and also prevent clots from forming and growing.

M201 (81 decks)

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