- Shuffle
Toggle OnToggle Off
- Alphabetize
Toggle OnToggle Off
- Front First
Toggle OnToggle Off
- Both Sides
Toggle OnToggle Off
Front
How to study your flashcards.
Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key
Up/Down arrow keys: Flip the card between the front and back.down keyup key
H key: Show hint (3rd side).h key
![]()
PLAY BUTTON
![]()
PLAY BUTTON
![]()
76 Cards in this Set
- Front
- Back
|
Which hormones can affect blood pressure?
|
Circulating hormone: catecholamines, ANP, renin, aldosterone
Local hormones: autacoids (prostaglandins, nitric oxide, endothelin) |
|
Which hormone has been implicated in the genesis of hypertension with phaeochromocytoma?
|
catecholamines
|
|
What is phaeochromocytoma?
|
A tumor of adrenal tissue, usually at the medulla
|
|
How does defective renal sodium excretion cause hypertension?
|
Inhibiting tubular and vascular smooth muscle Na+/K+ase, which elevates intracellular calcium --> vasoconstriction
|
|
What is the BP target with medication for those with hypertension with concomittant diabletes, renal disease or arterial disease?
|
<130/80mmHg
|
|
What percent reduction in risk factors for stroke and CHD occur when giving pharmacological intervention to those with hypertension?
|
40% less stroke risk, 15% less CHD risk
|
|
What are the two types of calcium channel antagonists?
|
dihydropyridines, non-dyhydropyridines
|
|
t/f... Nifedipine-like drugs act exclusively on vascular smooth muscle, lowering BP by vasodilation, whereas verapamil and diltiazem have additional effects on the heart, reducing AV nodal conduction and myocardial contractility.
|
true
|
|
What suffix do ACE inhibitors end in?
|
pril
|
|
What does angiotensin II do to blood vessels?
|
vasoconstrict
|
|
Which ACE inhibitors are not prodrugs?
|
captopril, lisinopril
|
|
How are ACE inhibitors are prodrug?
|
Need to be converted in the liver to their active diacid metabolite
|
|
When are thiazides contraindicated, and what side effects do they produce?
|
metabolic side effects, eg hypokalaemia, hyperglycaemia and hyperuricaemia
avoid in patients with diabetes or gout |
|
t/f... thiazides solely reduce BP through natriuresis and diuresis.
|
false, also have a direct vasodilatory effect
|
|
How do beta adrenoceptor antagonists lower BP?
|
lower cardiac output
|
|
When are beta blockers contraindicated?
|
obstructive airway disease, diabetes, peripheral vascular disease
|
|
Name two selective b1 receptor antagonists?
|
atenolol, metoprolol
|
|
t/f... clonidine and methyldopa are vasodilators
|
false. they decrease sympathetic outflow centrally.
|
|
Name two drugs that are alpha-1 andrenoceptor antagonists, and what their effect is
|
prazosin, terazosin: vasodilate
|
|
What changes do the arterial baroreceptor reflex compensate for?
|
changes in posture, metabolic activity or external threats triggering sympathetic reactions
|
|
Where are the baroreceptors located?
|
carotid sinus and aortic arch
|
|
What are arterial chemoreceptors primarily stimulated by?
|
pO2 of arterial blood
|
|
Where do the arterial chemoreceptors mainly detect changes?
|
in the low pressure part of the circulation (left and right atria)
|
|
t/f... antidiuretic hormone released during hemorrhage is the work of the arterial chemoreceptors
|
true
|
|
What are risk factors for hypertension?
|
diet (primarily salt, but also other dietary components such as potassium and fish oils), obesity, ethanol, lack of exercise and stress
|
|
In basic life support, what is the ratio of compressions to breaths?
|
30:2
|
|
How might an adrenal tumor cause secondary hypertension?
|
overproduction of aldosterone
|
|
What is cardiac arrest?
|
no CO
|
|
What is asystole?
|
no electrical activity
|
|
What is it called when the heart is beating at 300/min
|
ventricular flutter
|
|
What is the emergency treatment for bradycardia with syncope?
|
beta1 adrenergic stimulant (isopropyl or noradrenaline), then electrical pacing
|
|
What pharmacological agents are important to consider in taking a history of hypertension?
|
oral contraceptive pill, NSAIDs, nasal decongestants, corticosteroids, appetite suppresants, anti-depressant MAO inhibitors, cyclosporin, erythropoeitin
|
|
What are the obligatory tests for suspected hypertension?
|
urinalysis (blood, protein, glucose), urine sediment (exam and culture), plasma EUC, LFT, thyroid function, FBC, CXR (heart size, rib notches), ECG
|
|
What do you test for Conn's Syndrome?
|
plasma aldosterone/renin ratio
|
|
What are the three largest causes of secondary HT?
|
OC pill (40%), renal parenchymal disease (30%), renovascular disease (20%)
|
|
t/f... Transplantation of a kidney from a hypertensive donor into a normotensive recipient does not cause HT
|
false, it does cause HT
|
|
What is the inheritance pattern of Liddle's Syndrome?
|
autosomal dominant
|
|
How does Liddle's Syndrome cause HT?
|
excess reabsorption of Na in the renal tubules, leading to K+ and H+ loss, which causes HT, hypokalaemia, alkalosis and low plasma renin
|
|
What is mild hypertension?
|
140-150/90-99 mm Hg
|
|
What are the side effects of ACE inhibitors and why?
|
dry cough (bradykinin a substrate for ACE)
increase in serum K+ (less aldosterone) worsen renal function (if already impaired) anaphylaxis (rare - related to bradykinin) contraindicated in pregnancy (2.7x risk foetal malformation) |
|
How does angiotensin II increase fluid retention?
|
releases aldosterone --> Na+ retention --> fluid retention
|
|
What type of drugs are sartans?
|
angiotensin II antagonists
|
|
What angiotensin II (AT) receptor subtypes exist in humans?
|
AT1, AT2
|
|
Which is more effective in lowering BP - AT1 antagonists or ACE inhibitors?
|
they are equally effective
|
|
t/f... an AT antagonist side effect is dry cough
|
false, as bradykinin is able to be metabolised by ACE
|
|
What Ca channels do Ca channel blockers act on, and how does that effect VSMCs?
|
L-type. relaxes VSMCs
|
|
What are ca channel blocker side effects?
|
peripheral oedema, constipation, decreased CO (--> heart failure)
|
|
How do thiazide diuretics work?
|
they block Na+ reabsorption
|
|
Where do thiazides act?
|
distal convoluted tubule
|
|
what does thiazide's effect on VSMCs do to TPR?
|
lowers peripheral resistance
|
|
What are the side effects of thiazides?
|
gout (uric acid), hypercalaemia (Ca2+) hypokalaemia (K+)erglycaemia
|
|
How do beta-adrenoceptor blockers inhibit renin release?
|
block CNS sympathetic flow
|
|
What are the side effects of beta blockers?
|
bradycardia, muscle fatigue, cold hands and feet, bronchospasm, diabetes (when combined with thiazides)
|
|
How effective is atenolol? and with a diuretic as well?
|
50-60% --> 60-80%
|
|
What are contraindications for beta adrenoceptor antagonist?
|
asthma, peripheral vascular disease, heart failure (bradycardia)
|
|
What is the sodium restriction for appropriate lifestyle modification for hypertensive patients?
|
<4mg/day
|
|
What are the three first line treatments for uncomplicated hypertension?
|
ACE inhibitors (or AT blockers), dihydropyridine ca channel blockers, thiazide diuretics (in >65 years)
|
|
When should a second agent be used in hypertension?
|
minimal response to single agent, or failure to get down to target BP
|
|
When should drug doses be increased in hypertensive medications?
|
after 2nd drug is added, and still not at target BP
|
|
How many patients are on 2+ drugs for their hypertension?
|
50-75%
|
|
How is obesity defined in men and women?
|
>25% body fat in men, >35% body fat in women
|
|
what is an overweight BMI?
|
25-29 kg/m^2
|
|
What is an obese BMI?
|
>30 kg/m^2
|
|
How many Australian adults are overweight and obese respectively?
|
60% overweight
20% obese |
|
How many Australian children are overweight and obese respectively?
|
20% overweight
5% obese |
|
How does hyperinsulinaemia affect BP and CVD risk?
|
BP: it directly increases sympathetic activity.
CVD risk: it decreases adrenal medullary activity --> decreasing HDL cholesterol |
|
what happens to leptin as a person becomes more obese?
|
leptin levels increase, but the person becomes more insensitive to its effects
|
|
What are the effects of atherogenic dyslipidaemia?
|
increased serum triglycerides
increased apolipoprotein B increased small LDL reduced HDL |
|
Which cardiomypathy is associated with obesity and why?
|
eccentric hypertrophy, due to increased intravascular volume
|
|
What is Sydrome Z?
|
Syndrome X + obstructive sleep apnea
|
|
Where is renin released?
|
kidney juxtaglomerular cells
|
|
Where does angiotensin II act on the brain, and what does it release?
|
posterior pituitary; ADH
|
|
What happens to arterial pressure if intake of salt and water is increased?
|
increased arterial pressure
|
|
How can renal sympathetic nerve activity affect the renal function curve?
|
increasing renal vascular resistance, increasing sodium reabsorption, increasing renin release
|
|
What is a way of increasing long-term activity of renal sympathetic nerve activity (RSNA)?
|
chronic resetting of baroreceptor reflex
|
|
What non-baroreceptor mechanisms could increase long-term RSNA?
|
chemoreceptor input from chronic intermittent hypoxia (ie. OSA)
angiotensin II acting on circumventricular organs of the brain (but can't cross blood brain barrier) leptin/obesity: also control sympathetic outflow |