Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cardio Exam 1 > Lecture 3 > Flashcards

Lecture 3 Flashcards

1
Q

protein

A

a macromolecule with large AA sequence (50 to several hundred AA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

peptide

A

a short AA sequence (up to 20-30 AA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

proteolytic enzyme AKA protease AKA peptidase

A

an enzyme that cleaves peptide bonds in peptides & proteins

chops peptide bonds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

receptors

A

proteins (usually located on the plasma memb) to which ligands bind and cause certain effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Angiotensinogen

A

precursor of all angiotensins
inactive
continuously secreted by the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Renin

A

protease that is made by juxtaglomerular cells
converts angiotensinogen to angiotensin I
rxn is a RATE LIMITING STEP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Angiotensin I

A

inactive

formed in systemic cirulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

ACE (angiotensin converting enzyme)

A

protease
on endothelial cells and circulating in blood
converts Ang I to Ang II
degrades bradykinin (potent vasodilator peptide) into inactive fragments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Angiotensin II

A

main active peptide of RAS
formed in systemic circulation
has 2 types of receptors (AT1 is the mediator of pressor effects)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Angiotensin 1-7

A

*peptide member of RAS
some of its effects are opposite to Ang II effects
*mediated through its own receptor (Mas receptor)
*can be formed from both Ang I or Ang II
*Ang I uses NEP to get to Ang 1-7
*Ang II uses ACE2 to get to Ang 1-7

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Regulation of renin release through long-loop negative feedback

A
  1. macula densa pathway
  2. intrarenal baroreceptor pathway
  3. beta-adrenergic receptor pathway
    * *increase in circulating Ang II –> decrease renin release
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

macula densa pathway

A

decrease NaCl flux across macula densa

Macula densa senses when the filtrate has low levels of NaCl, then it will stimulate the release of renin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

intrarenal baroreceptor pathway

A

decrease BP in afferent arteriole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

beta-adrenergic receptor pathway

A

activation of beta1-receptors on juxtaglomerular cells

release of renin will be stimulated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

short-loop negative feedback of renin release

A

stim Ang receptors on juxtaglomerular cells –> decrease renin release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

long-loop negative feedback of renin release

A

increase circulating Ang II –> increase BP –> decrease renin release

17
Q

What kind of receptors are AT1 and AT2 receptors?

A

G-protein coupled receptors

18
Q

What does Ang II do to the vasculature when AT1 is stimulated?

A

vasoconstriction

smooth muscle hypertrophy

19
Q

What does Ang II do to the adrenal cortex when AT1 is stimulated?

A

stimulates syn and secretion of aldosterone

20
Q

What does Ang II do to the adrenal medulla when AT1 is stimulated?

A

stimulates epinephrine release

21
Q

What does Ang II do to the kidney when AT1 is stimulated?

A

efferent arteriole vasoconstriction
inhibition of renin release
increased Na+ reabsorption

22
Q

What does Ang II do to the heart when AT1 is stimulated?

A

myocardial hypertrophy

collagen synthesis

23
Q

What does Ang II do to the brain when AT1 is stimulated?

A

release of vasopressin (=ADH)
stimulation of thirst and salt appetite
increased central sympathetic outflow

24
Q

ACE-I MOA

A
  1. decreased formation of Ang II
  2. increased circulating levels of bradykinin
  3. increased (indirectly) formation of Ang (1-7)

also increase renin levels/activity b/c the negative feedback of Ang II is not functional!
Binds to the binding site of ACE

25
Q

Effects of ACE-I in hypertensive patients

A
  • decrease vascular resistance & BP
  • increase the compliance of large arteries
  • (SLIGHT) decrease in GFR and/or filtration fraction
  • aldosterone secretion is (slightly) decreased –> risk for hyperK-emia!
  • cardiac function is usually unchanged
26
Q

Main ADR’s of ACE-I

A
  • hypotension
  • cough
  • hyperkalemia
  • acute renal failure (in predisposed patients)
  • modest elevation of serum creatinine
  • combo w/ NSAIDs leads to decreased GFR
  • teratogenic effect
  • angioedema
27
Q

AT1 receptor antagonists/blockers (ARBs) MOA

A
  • arterial vasodilation & reduction in peripheral resistance
  • reduction of serum aldosterone levels
  • inhibition of peripheral sympathetic activity
  • improvement of hemodynamic profile in heart and kidney
  • increased renin release
  • increased Ang II levels in plasma
28
Q

ADRs of ARBs

A
  • hypotension
  • less angioedema than ACE-I
  • hyperkalemia
  • teratogenic
29
Q

Aliskiren MOA

A

renin inhibitor

30
Q

ADR’s of Aliskiren

A
  • headache, fatique, dizziness
  • diarrhea
  • nasopharyngitis, epitaxis (nosebleed)
  • hyperkalemia
  • hyperuricemia
  • teratogenic

Cardio Exam 1 (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions