Brainscape's Knowledge GenomeTM

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


See full index

(DIT) Rapid Fire + 4/5 Stars > Blood Pressure > Flashcards

Blood Pressure Flashcards

1
Q

Sympathetic BP control mechanism

A

Short term BP control, reacts rapidly to hypotension
Baroreceptors – stretch in vessel wall
-carotids, aortic arch
–>medullary vasomotor center
–>sympathetics, increase vasoconstriction, increased HR

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

Aortic arch vs carotid sinus baroreceptor signaling

A

Aortic arch – signal to solitary nucleus via CN X

Carotid arch – signal to solitary nucleus via CN IX

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

Baroreceptor response to hypotension

A

Decreased BP = less stretch

  • > decreased afferent baroreceptor firing
  • solitary nucleus decreases efferent parasympathetic stimulation – Vagus N.
  • Increase efferent sympathetic stimulation
  • > increased alpha1 vasoconstriction
  • increase HR and contractility via beta 1 receptors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Baroreceptor response to hypertension

A

Elevated BP = increased arterial stretch

  • > increased afferent baroreceptor firing
  • > solitary nucleus increases parasympathetic stimulation -> decreased HR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Cushing’s reflex

A

Increased intracranial pressure
Constricts arterioles in brain -> cerebral ischemia

Hypothalamus stimulates SNS -> alpha 1 vasoconstriction

Triad:
Elevated BP
Reflex bradycardia – d/t baroreceptor stretch
Respiratory depression

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

Carotid massage to dx SVT

A

Increases stretch in carotid
Tricks body into thinking BP high -> decreased HR
Able to see underlying heart rhythm on EKG

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

Draw out vasoconstriction physiology

A

Page 202

Cause relaxation:

Via endothelial cell action:

  • bradykinin
  • ACh
  • alpha2 agonists
  • Histamine
  • Serotonin
  • Shear stress

Via sm.m. cell action:

  • Nitrates
  • LPS
  • Ca2+ CCB – dihydropyradines
  • Epinephrine (b2)
  • Prostaglandin E2
  • Sildenafil – PDE5 inhibitors
  • BNP and ANP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Peripheral chemoreceptors

A

Respond to:
Hypoxia
Hypercapnia
Acidosis

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

Central chemoreceptors

A

Surface of medulla

Respond to changes in CO2 and pH in CSF not blood

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

Chemoreceptor primary mechanism

A

Primarily affect respiratory rate

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

Atrial natriuretic peptide (ANP)

A

Hormone produced in atria in response to:

  • Increased atrial volume
  • Increased atrial pressure

Vasodilator

Natriuretic peptide – diuresis

  • act on afferent and efferent arterioles of renal glomeruli
  • constrict efferent, dilate afferent -> increased GFR
  • promotes diuresis
  • decreases BP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Autoregulation – heart

A

Mediators: CO2, NO, adenosine

Underperfused:

  • CO2 -> dilated coronary a.
  • NO -> dilated coronary A

In ischemia already max dilated
Nitroglycerine causes systemic venous vasodilation
-reduces preload -> decreased myocardial O2 demand

Adenosine = energy starved state

  • potent vasodilator
  • > flushing reaction w/ IV push
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Autoregulation – lungs

A

Hypoxia -> vasoconstriction

-delivers pulmonary circulation to well oxygenated areas of lungs

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

Diagnosing HTN

A

BP >= 140/90 on 3 or more different occasions

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

Risk factors of HTN

A 
Age
Smoking
Excess etOH
Excess Na+ intake
Physical inactivity
Obesity
DM
FHx
Race: AA > whites
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Causes of secondary HTN

A 
Renal a. stenosis MC
Chronic kidney disease or ESRD
Medications: OCP, NSAIDs, antidepressants, glucocorticoids
Illicit drugs – cocaine, amphetamines
Adrenal diseases:
-Hypercortisolism – Cushing syndrome
-Hyperaldosteronism – Conn syndrome
hypo/hyper thyroidism
Hyperparathyroidism
Coarctation of aorta
OSA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

HTN urgency vs emergency

A

Urgency: >= 180/120
-no end organ damage

Emergency: >= 180/120
-end organ damage: EKG changes, CP, HA, vision abnormalities, kidney, flash pulmonary edema

Tx:
IV nitroprusside – SE cyanide toxicity
IV labetalol

18
Q

Left ventricular hypertrophy

A

Increased BP -> increased afterload on LV
-> wall hypertrophy
S4 sound

Increased myocardial O2 demand

  • more tissue to oxygenate
  • thicker doesn’t mean stronger -> stiffer, less compliant

LV holds less blood during diastole

Precursor for left sided HF and MI

19
Q

Aortic dissection

A

Tear of intima of aorta – blood dissects into wall of vessel -> false lumen

Causes:

  • HTN – MC
  • Dz of aorta (e.g. cystic medial necrosis in Marfans)

Ascending aorta
Tearing chest pain, radiates to back

CXR: widening mediastinum

75% mortality if not tx early

Use b-blocker to decrease BP in HTN w/ aortic dissection
Decreases slope of rise in BP

20
Q

Stanford type A vs B aortic dissection

A

A:

  • Ascending aorta
  • tx surgically, emergency

B:
Confined to descending aorta
-“Below the branches”
-tx medically

21
Q

ACE inhibitors

A

-pril

inhibit ACE activation of AngII – prevents vasoconstriction

Increases bradykinin -> vasodilation

Decreases pre- and after-load

Use:
HTN, CHF, Post MI – prevent LVH remodeling
Kidney dz – reduce proteinuria, decrease progression of diabetic nephropathy

SE:
Cough, throat clearing d/t bradykinin
Angioedema – anywhere from lips to larynx
-> airway compromise; d/t bradykinin
hyperkalemia
mild renal insuffiency d/t slightly decreased GFR – increased serum Cr
Avoid in renal a. stenosis

Teratogenic

  • fetal renal dysfunction
  • oligohydramnios
  • fetal cardiac malformations
22
Q

Angiotensin receptor blockers

A

-sartan

inhibit AngII receptor
Same uses and SE as ACEI except no cough, still causes angioedema

Decreases pre- and after-load

23
Q

Aliskiren

A

Renin inhibitor

SE:
Hyperkalemia
Renal insufficiency
Contraindicated in pregnancy

Not indicated for CHF and MI, only HTN

24
Q

Nitrates

A

Nitroglycerin
Isosorbide dinitrate
Nitroprusside

Release NO -> venous relaxation, decreases preload

Tx: angina, acute pulmonary edema

SE:
Reflex tachycardia
Flushing
HA

Nitroprusside -> cyanide toxicity

25
Q

Dihydropyridine CCBs

A

Amlodipine, felodipine, nicardipine, nifedipine, nisoldipine

MOA: act on vascular sm.m. -> vasodilation

Use:
HTN
Angina
Vasospasm – Prinzmetal’s angina, Raynaud’s
Esophageal spasm
Migraine prophylaxis
SE:
Peripheral edema
Flushing
Dizziness
Constipation
Reflex tachycardia
26
Q

Nondihyropyridine CCBs

A

Diltiazem, verapamil

Block calcium channels at pacemaker cells

Use:
HTN
Angina
Arrhythmias

SE:
Cardiac depression – avoid in CHF
AV block
Flushing
Dizziness
constipation
27
Q

Minoxidil

A

Opens K+ channels -> hyperpolarize sm.m
-> relaxation of vascular sm.m.

Use:
Severe HTN
Topical application – hair loss

SE:
hypertrichosis
hypotension
reflex tachycardia
fluid retention/edema
28
Q

JNC8 BP goals

A

Over 60 w/o DM or CKD – less than 150/90

All others less than 140/90

29
Q

JNC8 initial pharmacotherapy for HTN in CKD pts

A

ACEI/ARB – renal protective

30
Q

JNC8 initial pharmacotherapy for HTN in Black pts w/o CKD

A

Thiazide diuretic

CCB

31
Q

JNC8 initial pharmacotherapy for HTN in Non-black pts w/o CKD

A

Thiazide diuretic
CCB
ACEI/ARB

32
Q

Initial tx option/avoid in HTN plus CHF

A

ACE/ARBs
b-blocker (carvedilol, metoprolol, bisoprolol)
aldosterone antagonist

Avoid: CCB, b-blocker if acute decompensated CHF or cardiogenic shock

33
Q

Initial tx option/avoid in HTN plus DM

A

ACE/ARB

Avoid b-blocker – masks hypoglycemic effects

34
Q

Initial tx option/avoid in HTN plus Post-MI/CAD

A

Thiazide, b-blocker, ACE/ARB – decrease mortality

CCB, Nitrates – for angina

35
Q

Initial tx option/avoid in HTN plus afib

A

b-blocker, diltiazem/verapamil – slow heart

36
Q

Initial tx option/avoid in HTN plus bradycardia

A

Avoid b-blocker, diltiazem/verapamil (slows heart)

37
Q

Initial tx option/avoid in HTN plus BPH

A

Alpha-blocker

38
Q

Initial tx option/avoid in HTN plus pregnancy

A

Hydralazine
Methyldopa
Labetalol
Dihydropyridine CCB

Avoid: ACE/ARBs

39
Q

Initial tx option/avoid in HTN plus migraines

A

CCB

b-blocker

40
Q

Initial tx option/avoid in HTN plus essential tremor

A

Propranolol

41
Q

Hydralazine

A

Increased cGMP -> stimulation of myosin phosphatase -> arterial relaxation, decrease afterload

Use: HTN urgency/emergency, HTN in pregnancy

SE:
Reflex tachycardia
Caution in CAD -> increased O2 demand
Fluid retention
Nausea
HA
Drug induced lupus
42
Q

Antihypertensives safe in pregnancy

A

“Hypertensive Moms Love Nifedipine”

Hydralazine
Methyldopa
Labetalol
Nifedipine or other dihydropyridine CCB

(DIT) Rapid Fire + 4/5 Stars (162 decks)

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