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Pharmacology > Week 5 & 6 > Flashcards

Week 5 & 6 Flashcards

(65 cards)

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1
Q

Hyper tension stages + systolic and diastolic pressure

A

Pre HT: over 120S or 80D
Stage 1 HT : over 140S , or 90D
Stage 2 HT: Over 160 S or 100 D
HT Crisis: OVer 180 S or 110 D

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2
Q

Complications of Uncontrolled HyperT

A

Heart failure
Brain Strokes , TIA
CKD
Peripheral vasc disease
Retinopathy

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3
Q

What can prolonged Hyper do to the left ventricle

A

Cause thickening of muscle wall.

loss of elasticity and strength.

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4
Q

Common area for plaques to break off and cause TIA in the brain?

A

CC Aa. bifurcation

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5
Q

What acts as an observable symptom of Hypertension

A

retinopathy (cotton wool white spots on eye)

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6
Q

What causes 95% of Hyper tension

A

Essential/ Primary , idiopathic Hypertension .

links to genetics but caused by RISK FACTORS

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7
Q

Secondary Hypertension is linked to what?

A

underyling health condtions such as renal diseases and endocrine disorders.

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8
Q

two types of HypeT risk factors

A

modifiable and non modifaible

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9
Q

Commonly taken drugs that increase risk of HyperT

A

NSAID, contraceptives, C.steroids, Stimulants, oral-decongestants

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10
Q

Main changes to diet to reduce CV Hypertension risk

A

Reduce salt intake

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11
Q

What BP should we aim for when reducing Hypertension

A

as low as tolerable

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12
Q

Approach to reduce Hypertension

A

Inhib RAAS

Reduce fluid vol (duiretics)

Cause vasodilation (vasodilators)

inhib. sympa system : alpha and beta blockers

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13
Q

endings for ACE inhibs

A

-pril

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14
Q

what is the main troublesome side effect of ACE inhibs?

A

inhibit bradykinin release -> dry cough
Hyperkalaemia (high potassium levels)
Angiodema

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15
Q

management of angiodema

A

d/c RAAS inhib.

antihistamine &/ adrenaline/ steroids & airway management

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16
Q

Generic name ending for AGT2 antagonists

A

-artan

“sartans”

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17
Q

When are AGT2 antagonists typically used?

A

when Pt. cant tolerate ACE inhibs (typically due to bradykinin inhib)

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18
Q

main adverse effects of AGT2 antag

A

Hyperkalaemia

more sus. to angiodema if already occured with ACE inhib.

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19
Q

3 main groups of diuretics

A

Thiazides

K+ sparing

Loop

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20
Q

which diuretic is first choice for treating HyperT

A

Thiazides

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21
Q

function of thiazides

A

increase excretion of na+,K+,Cl-, H+ (and therefore water)

vasodilation at low doses
can produce HYPOkalaemia.

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22
Q

Main function of K+ sparring (amiloride)

A

increase na+ and Cl- but not K+ secretion

can produce HYPERkalaemia

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23
Q

Main function of Loop diuretics?

A

Prevent reabsorption of na+ and k+ at loop of Henle

LARGE increase in secretion of those ions.

can produce HYPOkalaemia

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24
Q

Why are diuretics banned in sport

A

hide use of steroids through increased secretions

drop body weight, useful for prize fighters, jockeys and bodybuilders.

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25
Smooth muscle calcium channel blockers
nifedipine, amlodipine, felodipine
26
Myocardium calcium channel blockers
verapmil, dilitazem
27
what do most direct vasodilators do?
dilate both Aa. and Vv.
28
What are minoxidil and hydralazine used for?
ARTERIOL selective vasodilators. orally used in conjuction with B blocker and diuretics
29
main used of sodium nitroprusside
emergency use , rapid acting, IV only. can rapidly drop BP and cause rebound tachycardia so often used in conjuction with B blockers
30
selective A blockers name ending
-osin
31
what drugs are prazosin and terazosin
A blockers
32
main use of A blockers
block peripheral A1 receptors Benign prostatic hyperplasia
33
drug pathway for newly diagnosed hypertension
1. inhib RAAS or Calcium channel blocker or diuretics (65 +) 2. if target BP not reached: inhib RAAS + calcium channel blcoker or inhib RAAS and low dose thiazide diuretic 3. if BP still not reached: inhib RAAS + low dose thiazide + calcium channel blocker 4. if BP still not reached : seek specialist advice.
34
drugs contraindicated for COPD and asthma when treating HyperT
B blcokers (cardioselectives can be sued with caution)
35
drugs contraindicated for 2nd or 3rd degree heart block when treating HyperT
B blockers, dilitazem and verapamil
36
drugs contraindicated for heartfailure when treating HyperT
Calcium channel blcokers (especially dilitiazem and verapamil)
37
drugs contraindicated for GOUT when treating HyperT
Thiazide diuretics (increase uric acid of gout)
38
why does the addition of NSAID with RAAS inhibs and diuretics cause the triple whammy effect.
AGT2 is blocked so no vasoconstriction of AFFERENT arteriole. diuretics will cause loss of ions and fluids in urine. decrease blood volume and perfusion in kidneys NASAID block prostaglandins dilatory effect on AFFERENT arteriole. OVERALL reduced blood flow to kidneys
39
main thereputic manipulations of endocrine system
hyper/hypo secretion loss of response to hormone using it to treat non endocrine problem
40
which hormone is more physiologically active T3 or T4?
T3
41
what is released from hypothalmus and pit. gland to eventually allow release of thyroid hormones
Thyroid releasing hormone (Hthalamus) Thyroid stim hormone (pit. gland).
42
main causes of hypothyroidism
Hasimotos thyroidism postpartum thyroidism iodine def. anti-thyroid drugs thyroid surgery thyroid irradiation
43
how are T4 or T3 administered as a drug?
orally
44
why is T4 preferred over T3?
longer 1.2 life
45
what is main problem with administering drugs with patients with hypoTHyroidsm?
decreased GIT function means the orally T3/4 tabelts arent introduced into system effectivly + poor metabolic rate means drug isnt cleared well. so we need to inhib CYP450 to allow better met. of T3/4/
46
drugs which increase THYROID BINDING GLOBULE (TBG)
Oestrogens, tamoxifen, methadone
47
Drugs which decrease (TBG)
Thyroid binding globule Androgens, glucocorticoids
48
Main diseases causing Hyperthyroidism
Graves disease and multinodular goitre
49
physiological process behind graves disease
Autoimmune: bodies antiB fit in TSH receptors creating abundance of T3 and T4. the problem is too much T3/4 not too much TSH (as antiB are just mimicing this function).
50
Main physiological process behind multinodular goitres
abnormal nodules create T3/4 in an uncontrolled manner. low TSH high T3/4
51
common thionamindes?
carbimazole and propylthiouricil
52
main treatment for hyperthyroidism?
Thionamides radioiodine surgery B blockers (prior to therapy)
53
how do thionamides work?
stop uptake of iodine into thyroid hormone
54
adverse effects of thionamides
3-4 weeks to take effect. pruritus and rashes
55
function of exocrine
secreate hormone into ducts e.g. pancreatic duct.
56
Functions of endocrine cells:
secreate hormones into blood e.g. islets of langerhans
57
Hormones that increase Blood glucose
glucagon adrenaline cortisol (stress hormone) growth hormone
58
hormones which decrease blood glucose
Insulin
59
effects of insulin
increase uptake of Glucose in skeletal muscles and fat tissue glycogenisis in liver Spare glucose converted into fat Amino acid uptake in cells decrease lipolsys in fat cells
60
How does insulin effect a cell
binds to its own insulin receptor causes more glucose channels to insert on cell membrane insulin then changes gene expression in cell and alter metabolism and transport.
61
which two organs do not depend on insulin
heart and brain. they do not contain insulin receptors and have other sources for glucose uptake.
62
what is glycosuria
high glucose in urine
63
what is osmotic diuresis
extra glucose in urine causes excess water to be pulled into urine meaning diabetics urinate often and are thirsty often
64
why is protein catabolism a negative function for diabetics?
proteins -> smaller amino acids mean glucose neogenisis will be stimulated. Amino acids converted into glucose
65
why are diabetics also more likely to develop ketoacidosis
increased lipolsysis will cause ketones as a by product.

Pharmacology (6 decks)

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