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biom3020 > THOMAS cardiovasc > Flashcards

THOMAS cardiovasc Flashcards

1
Q

What is metabolic syndrome

A 
Central obesity
High BP
high triglycerides
low HDL cholestorol
Insulin resistance
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2
Q

HOw to control Bp

A

3 Ways to increase blood pressure•↑ rate/strength of heart to ↑volume through vessels•↓ diameter of blood vessels to ↑ flow•↑ retenƟon of water/salt to ↑ blood volume

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3
Q

Early treatment of bp?

A

Low salt diet•Sympathectomy/adrenalectomy•Antimalerial(pentaquine

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4
Q

bp lower drugs

A

phenoxbenzamine SN blocker |->Dizziness tachycardia

guanethidine -> adrenergic inhibitor Hypotension sexual dysfunction diarrhoea

reserpine-> sedative |fatigue insomnia depression

hydralazine-> vasodilator |headaches tachycardia

propranololBeta blocker(s) Dizzinessinsomnia impotence

verapamilCalcium channelblockers

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5
Q

Diuretics

A

Kidney
‐filters ¼ of cardiac output/min‐Salt -rheostat and water follows salt

Antibiotic sulfanilamideleads to salt in urine
•1957 Chlorothiazide↑ salt in urine in dogs
•↓ BP in humans and ↓ risk by 1/3 of stroke/MI/HF/renal damage

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6
Q

Beta and calcium channel blockers

A

↓ load on/rate of heart ↓ angina
Adrenaline can ↑ rate/strength of heart

Therefore if you block adrenaline, can decrease load on heart
But how to do this specifically in heart?

1948 discovered alpha and beta adrenergic receptors
beta is in heart
→ propanolol
↓ angina and also ↓ BP

Research → verapamil (not beta blocker)
Verapamil block calcium entry in cells
Ca2+contracts cells
Relaxs blood vessels and ↓ BP

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7
Q

what did goldblatt work out

A

Patients with hypertension had narrowed blood vessels in kidney.

Would constriction of renal artery cause hypertension?
1934 one kidney clamp in dogs↑ BP

Model of hypertension
He suspected “renin”

if you clamp kidney bp increase by releasing renin

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8
Q

How does losartan work?

A

if you have normla blood pressure if you take losartan doesnt decrease, (at1 receptor blocker)

Relaxes blood vessel
Hypertensiec phenotype is renin agiotensin overactivity

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9
Q

mechanisms of hypertension

A

RAS is upregulated, create more angioteniss, constrict blood vessels

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10
Q

rat and human RAS relationship?

A

human angiotensinogen, isnt recognized by mouse and vice versa

Transgenic mice are humanized

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11
Q

LOCAL RAS

A

Local tissue system capable of generating AngII independent of the circulating RAS.

angiotensinogen is everywhere

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12
Q

Angiotensinogen in brain

A 
Angiotensinogen
•Mostly in astrocytes•Some neurons•In situ/IMC•Angiotensin generated in CNS
•AT1R/AT2R behind BBB
•ACE in brain
•Renin where???

its in olfactory!

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13
Q

Angiotensinogen in brain

A 
Angiotensinogen
•Mostly in astrocytes•Some neurons•In situ/IMC•Angiotensin generated in CNS
•AT1R/AT2R behind BBB
•ACE in brain
•Renin where???

its in olfactor
its in hypoth and medulla-> stress response!

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14
Q

RAs in adrenal?

A

RAS in volved in growth and developement

Animals which and hasnt AT2 receptor,

cortex exprss type 1
medulaa express type 2

Losartan blocks type 1 in cortex but stillshows medulla

Function – ↑ aldosterone; adrenal development and growth

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15
Q

RAS in kidney

A

Renin present outside JG cells (proximal tubule/collecting duct)AngIIgeneration in kidney higher than blood!

FunctionRenal development, glomerular blood flow, tubular sodium reabsorption, and renin secretionTransgenic/transplantation

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16
Q

How can we examine organ specific effects of RAS?

A

Local gene delivery/overexpression- delete or knockout orr add in places

Cross transplantation- kidney

Cell‐specific gene activation/deletion

17
Q

RAS and Brain

A

Response to systemic
AngII seem to involve CNS•thirst•salt appetite
•Vasopressin release
•Sympathetic vasomotor activity

when injected mutant at1r in RVLM BP increased

when trangsenic mice which hus human angiotensigen expressing everywjere and put it in bloodstream you get raise in bloos pressure

renin is in nerve angGIN is everywhere
nerves have at2 so the whole cycle of anggin to ag2 has to happen, ACE expressed transmembrane

18
Q

local RAS in kidney

A

ang 2 acts on kidney to increase sodium retention

cross transplantation of kidneys between at1r KO mice and wile type

loss of at1r in kiden alone can significantly reduce ang2 induced hypertension

when KO apart from kidney, sustained increase in hypertension are driven by kidney

when kidney knockout -> goes back to normal -> kidney crucial for long term BP regulation

19
Q

ACE2

A

Homolog to ACE, not inhibited by captoprilHigh amounts in heart and kidney40% homology to ACE HPLC/ms‐carboxypeptidasefor AngIand AngII

converts into angI 1-9 and ang2 1-7

AngI/AngIIconversion to Ang1‐9/Ang1‐7 ↓BPACE2 overexpression ↓BP in hypertensionACE2 KO –CV actions/injury ‐controversial Recombinant soluble ACE2 as therapeutic

20
Q

draw out model of cardiac RAS

A

hh

21
Q

Functions prior to RAS/BP

A

ACE/ACE2 in bacteria; appears in tunicates –horizontal transferACE from insect to mouse ‐fertility and developmentpeptide processing in Drosophila seminal fluidMosquito –ACE activates embryogenesis after blood mealFreshfly–ACE activity in ovariesACE in germ cells in mice –KO → inferƟlity

22
Q

RAAS survival advantageous

A

A highly active RAAS was of advantageous because salt and waterhomeostasis were important for survivalDramatic change to terrestrial life require efficient systemsTrue for H sapiens until we become domesticated and argiculturalSalt used for conservation of food → excess salt in dietRAAS in constant overdrive → hypertension → etcMismatch between evolution efficiency and availability is why ~50% of adults are hypertensive

23
Q

polymorphisms in RAS genes

A

Pharmacogenomics –promise vs reality1000 genomes (http://www.1000genomes.org) 38M SNPs individuals have 76–190 raredeleterious non‐synonymous variants and up to 20 LOF and disease‐associated variants.Reasonable hypothesis = RAS SNPs → hypertensionRAS genesAo, renin, ACE, ACE2, renin receptor, AT1R, AT2R, MASenzymes/receptor related to aldosterone

24
Q

Other actions RAS

A

huh

25
Q

Cre/Lox RAS and the kidney

A

proximal tubule influence blood pressure, by local production of

26
Q

What is Primary aldosteronism?

A 
Autonomous and inappropriate
secretion of aldosterone
Activation of distal tubular
sodium retention pathways
• HYPERTENSION
• SUPPRESSION
OF RENIN
• HYPOKALAEMIA
Potassium loss
Treatable by adrenalectomy in the case of aldosterone producing
adenoma or mineralocorticoid receptor antagonists in bilateral disease

Primary aldosteronism is a common cause of hypertension
• Hypokalaemia is a red flag but only present in 20-40%
• Screen with an aldosterone/renin ratio but be careful of the
pitfalls
• There is a strong rationale for screening and specifically
treating PA, due to adverse effects on CVS disease and renal
effects
• Awareness among primary care doctors is low and current
rates of screening are poor

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