W10 Hypertension Flashcards
(128 cards)
1
Q
In what 2 ways does ANS control BP in the arteries and arterioles over the short term ?
A
- by vasoconstriction or vasodilation
- by altering cardiac output
2
Q
How is BP regulated over the long term ?
A
Modulation of solute and volume through feedback loops that involve the hypothalamus, pit gland, adrenal cortex and the kidneys
3
Q
Where is SNS mediated vasoconstriction most powerful ?
A
Kidneys, intestine, spleen and skin
4
Q
What is the effect of vasoconstriction on blood flow?
A
Shifts blood from pelvis and lower extremities to the right heart —> increased end diastolic volume —> increased force of contraction —> increased SV —> increased CO —> increased BP
5
Q
What are chronotropic effects mediated by ?
A
B1- adrenergic receptors
6
Q
Afferent sensory fibres from the carotid sinus and aortic arch baroreceptors travel via _______
A
The glossopharyngeal (CN IX) and vagus nerve to postolateral medulla and Lower pons
7
Q
Increased carotid artery and aortic pressure response
A
Decrease sympathetic output, increased parasympathetic output —> decrease BP
Negative feedback loop = baroreceptor reflex
8
Q
Response to increased afferent arteriole pressure
A
Inhibits release of renin from JG cells —> decreased BP
9
Q
What is the effect of NPs on the kidney ?
A
Increase GFR —> natiuresis and diuresis
Decrease renin release —> further renal Na+ and water excretion, reduced vascular resistance
—> decrease BP
10
Q
What does accumulation of CO2 and H+ in the Brain cause ?
A
Vasodilation
11
Q
What does depletion of O2 and CO2 in the brain lead to ?
A
Vasoconstriction
12
Q
What is rarefaction of a vessel ?
A
When a vessel becomes functionally useless
13
Q
What happens to small arteries in patients with hypertension ?
A
Inward hypertrophy
14
Q
Causes of secondary hypertension (As)
A
Accuracy
(Sleep) Apnea
(Primary) Aldosteronism (commonest cause of secondary hypertension)
- decreased K+ is sign (but labs often come back normal)
15
Q
Causes of secondary hypertension (Bs)
A
Bruits (renovascular hypertension) - poor renal blood flow - renal artery stenosis Bad kidneys - chronic kidney disease
16
Q
Causes of secondary hypertension (Cs)
A
Catecholamines (pheochromcytoma) - tumour of adrenal medulla - fluctuations in BP Coarctation of the aorta - BP high in upper limbs, low in lower limbs Cushing’s syndrome - tumour of pituitary gland - increased aldosterone and cortisol
17
Q
Causes of secondary hypertension (Ds)
A
Diet: DASH diet
(Prescription) Drugs
- prednisone, Motrin, Advil, naproxen
(Street) Drugs
18
Q
Causes of secondary hypertension (Es)
A
Erythropoietin Endocrine (thyroid and parathyroid) - compensatory mechanisms over correct —> high BP
19
Q
Progression of fundoscopy findings with hypertension
A
Hypertensive retinopathy: AV nicking
MOderate hypertension: hard exudates, hemorhages
Pappiledema: blurring of the optic disc
20
Q
Why is auto regulation important to consider when treating hypertension ?
A
Have to lower BP over weeks to months so that blood flow can adjust, otherwise the patient may become hypotensive
21
Q
Hypertensive emergencies
A
Hypertensive encephalopathy Aortic dissection MI Left heart failure Intracranial hemorrhage Post-transplantation (of kidney) Post op
22
Q
Complications of hypertension
A
Stroke Coronary artery disease Peripheral vascular disease Kidney disease Sudden death
23
Q
Five key trends in healthcare
A
- Innovation in consumer technology market
- Advancement in electronic health records
- Shortage in health professional workforce
- Health system reorganization and financing
- Growth of consumerism of health care
24
Q
Lifestyle factors for uncomplicated hypertension
A
Aging Obesity and insulin resistance High salt diet Low potassium diet Sedentariness Stress
25
How does aging contribute to hypertension ?
Elastin replaced by collagen —> arterial stiffness —> widened pulse pressure —> isolated systolic hypertension
After ~ mid 50s
26
Why does arterial stiffness cause increased pulse pressure ?
Reflected systolic wave rebounds quicker and then contributes to systolic pressure instead of diastolic pressure like it should
27
What is the increased SBP with every 10% increase in weight ?
6.5mmHg
28
What % of hypertension fo weight gain and obesity account for ?
~25%
29
Mechanism of action for hypertension in obese and insulin resistant patients ?
Increase plasma volume and CO —> RAAS activation —> shifting of natriuresis to higher BP threshold in obesity —> SNS activation
30
What is Hypertension Canada recommended daily sodium limit ?
2g/day ~ 1 tsp salt ~ 5 g salt
31
What populations tend to be more sensitive to salt intake ?
Older
African Americans
Obese
Patients with metabolic syndrome or chronic kidney disease
32
What is the relation between potassium intake and BP
Inversely related
33
Why do diets rich in potassium help lower BP ?
Sodium excretion is diminished bu hypokalemia through increases in sodium reabsorption in proximal tubule and/or loop of Henle —> increased BP
34
What is work hypertension called ?
Masked hypertension: going to doctors office may be least stressful part of your day
35
What effect can >2 drinks per day have on hypertension
1.5 - 2 times more likely to develop hypertension than non-drinkers
36
How does excess alcohol consumption lead to hypertension ?
Stimulation of SNS, RAAS, raised cortisol levels, inhibition of nitric oxide
37
What are some other factors that can raise BP ?
```
Stimulants: cocaine
Decongestants: pseudoephedrine
Prednisone
Oral contraceptives
Some anti-depressants
NSAIDs
Supplements: St. John’s Wort, Ephedra, Ginko, Ginseng
```
38
Health behaviour changes to control hypertension:
Physical exercise (30-60 min moderate intensity, 4-7 days/week)
Weight reduction (BMI 18.5-24.9 optimal, waist circumfrance <102cm men, <88cm women)
Limit alcohol consumption: (<2/day, men <14/week, women <9/week)
DASH diet
Sodium reduction
Stress management via CBT and relaxation techniques
39
How does exercise help in management or prevention of hypertension ?
```
Increase endothelial production of NO synthase
Decrease aortic stiffness
Increase whole body insulin sensitivity
Reduce circulation noradrenaline
Decrease vascular resistance
```
40
What is the DASH diet ?
```
High in calcium, potassium and magnesium
Fruit and veggies
Low intake of red meat
Low fat dairy products
Plant protein
High fibre
```
41
What lifestyle change tends to have the greatest impact on BP ?
DASH diet
Normotensive: -3.6/-1.8
Hypertensive: -11.4/-5.5
42
What is criteria for hypertension in adults without diabetes ?
>140/90 mm Hg
43
What is threshold for hypertension in adults with diabetes ?
>130/80 mmHg
44
What is hypertension criteria for children and adolescents ?
S/DBP > 95th percentile for sex, age, BMI
45
When to suspect white coat hypertension
No TOD
Report lower out of office readings
Lightheaded or dizzy when started on antihypertensive therapy
46
What is normal BP for home/24 hour ABPM ?
24 hour average: <130/80
Daytime average: <135/85
Night time average: < 120/80
47
When to suspect masked hypertension ?
TOD present or LVH but normal office BP readings
48
Which type of hypertension puts a patient most at risk for CV events ?
Masked
49
When might someone be considered to be having a hypertensive emergency ?
BP >180/>120
| Depends on presence of progressive/acute TOD
50
What constitutes hypertensive urgency ?
Severely elevated BP without TOD the
51
Management of hypertensive urgency
Done in ER
Lower BP by 25% or <160/<100 over hours or over the day
Use normal BP meds or short acting meds (oral captopril, oral lasix or oral clonidine)
52
Common causes of hypertensive emergencies
```
Acute pulmonary edema
Stroke
MI
Acute aortic dissection
Acute renal failure
Hypertensive encephalopathy
```
53
What TOD can be seen with hypertension ?
```
Acute worsening of kidney function
Cardiac ischemia
Brain ischemia
Acute CHF
Acute aortic dissection
Papilledema
Stroke
Hypertensive heart disease
Hypertensive retinopathy
```
54
Investigations for acute worsening of kidney function
GFR
55
Investigations for cardiac ischemia
Signs and symptoms
ECG
Cardiac enzymes
56
Investigations for brain ischemia
Signs and symptoms (encephalopathy, acute stroke)
| CT or MRI
57
Investigations for acute congestive heart failure
Signs and symptoms
CXR
BNP
58
Investigations for acute aortic dissection
Signs and symptoms
| CT chest or echo
59
What % of strokes are attributable to hypertension ?
35%
60
What % of patients with heart failure have hypertension ?
80-90%
61
What does Hypertensive heart disease encompass ?
LVH
Heart failure
MI
62
What can be seen on fundoscopy in patients with mild hypertensive retinopathy ?
A-V nicking
63
What can be seen on fundoscopy in patients with moderate hypertensive retinopathy
Hard exudates
Flame shaped haemorrhages
Dot and blot hemorrhages
64
What can be seen on fundoscopy in patients with papilledema ?
Blurring of the optic disc
65
When is something considered a hypertensive emergency ?
Severely elevated BP with TOD
66
Treatment of hypertensive emergency
Aim to lower BP by 10-20% in first hour than further 15% over next 24 hours
Acute stroke: Lower to less than 185/110 mmHg if getting tPA otherwise only Lower if BP> 220/120
Acute dissection: rapidly decrease SBP to <120 mmHg in 20 minutes
67
What are standard investigations for patients diagnosed with hypertension ?
TOD: history and physical, ECG, GFR, urinalysis
Cardiac risk factors: history and physical, fasting lipid profile, ECG, weight, waist circumference, A1C or fasting blood glucose, UACR (if diabetic)
Secondary screen: history and physical, GFR, electrolytes, calcium, TSH
68
Who should be screened for secondary hypertension ?
Young patients
Patients with resistant hypertension
Patients that have clinical features of secondary hypertension
69
Cause of secondary hypertension
```
Obstructive sleep apnea
Chronic kidney disease
Renal artery stenosis/ Reno vascular disease
Fibro muscular dysplasia (FMD)
Primary hyperaldosteronism
Cushing’s syndrome
Pheochromocytoma
Thyroid disorders
Hyper parathyroidism
Acromegaly
Coarctation of aorta
```
70
How can Obstructive sleep apnea lead to hypertension ?
Sympathetic activity during periods of hypoxia —> excess aldosterone —> SNS activation
71
Screening tests for atherosclerotic RAS
CT angiogram
MR angiogram
Renal captopril scan
72
Screen tests for FMD
CT angiogram
| Digital subtraction angiography
73
Treatment of hyperaldosteronism
Idiopathic: mineralcorticoid receptor agonist
| Secondary to Adenoma or unilateral micro adenoma: may be cured with surgical adrenalectomy
74
How does the ratio of aldosterone to renin present in patients with hyperaldosteronism ?
High
75
Who should be screened for primary hyperaldosteronism ?
Resistant hypertension
Hypokalemia (although ~50% have Normal K)
Diuretic induced hypokalemia
76
Screening tests for hyperaldosteronism
Upright plasma aldosterone concentration and renin activity
77
What is Cushing’s Syndrome ?
Hypercortisolism usually from an adrenal tumour
78
Screening test for Cushing’s syndrome
1 mg overnight dexamethasone suppression test or 24 hour urine cortisol or late night salivary cortisol test (2/3 abnormal)
79
Clinical manifestations of Cushing’s syndrome
```
Proximal muscle weakness
Facial plethora
Fat deposition in scapular area or face
Central obesity
Thing fragile skin with easy bruising
Colourful stretch marks
Hirsutism, loss of libido
```
80
Signs and symptoms of pheochromocytoma
```
Episodes of:
Headaches
Palpitations
Diaphoresis
Panic attacks
Pallor
Hypertension
Or
These symptoms occurring with surgery, hard physical activity or injury
```
81
Screening for pheochromocytoma
24 hour urine fractioned metanephrines and catecholamines
82
Sign of hyperparathyroidism
Hypercalcemia
83
What are the classes of anti-hypertensive drugs ?
```
Diuretic agents
Inhibitors of RAAS
Calcium channel blockers
Adrenergic receptor antagonists
Direct vasodilators
Central acting agents
```
84
Different types of inhibitors of RAAS
ACE inhibitors
Angiotensin receptor blockers (ARBs)
Renin inhibitors
Aldosterone receptor antagonists
85
What suffix is used in ACE inhibitors ?
Pril (ramipril)
86
What is the mechanism of action of ACE inhibitors ?
Block conversion of Ang I to Ang II in the RAAS and block break down of bradykinin into its inactive form
—> inhibition of vasoconstriction
- inhibition of aldosterone secretion
- inhibition of NaCl reabsorption
- increased vasodilation (via Bradykinin)
—> decreased SVR and decreased preload
87
Adverse effects of ACE inhibitors
```
Cough (attributed to Bradykinin)
Hyperkalemia (due to reduced aldosterone )
Renal dysfunction
Hypotension
Angioedema (rare)
```
88
When are ACE inhibitors contraindicated ?
Pregnancy
| Renal artery stenosis
89
What suffix is used for ARBs ?
Sartan
90
Mechanism of action of ARBs
```
Antagonists that block the actions of Ang II
Inhibition of vasoconstriction
Inhibition of aldosterone secretion
Inhibition of NaCl reabsorption
—> decreased SVR and preload
```
91
Adverse effects of ARBs
Dizziness and hypotension
Hyperkalemia (due to reduced aldosterone)
Renal dysfunction
92
When are ARBs contraindicated ?
In pregnancy
93
Mechanism of action of renin inhibitors
```
Block conversion of angiotensinogen to Ang I
- inhibition of vasoconstriction
- inhibition of aldosterone secretion
- inhibition of NaCl reabsorption
—> decreased SVR and preload
```
94
Adverse effects of renin inhibitors
Diarrhea
95
Where are renin inhibitors contraindicated ?
In pregnancy
96
What is currently the only drug in the renin inhibitors class?
Aliskiren
97
Actions of calcium channel blockers
Decrease vascular smooth muscle contraction —> decrease SVR
Decrease cardiac conduction and contractility —> decrease HR, CO
Blocks Ca-signal to adrenal cortical cells to release aldosterone
98
Different classes of calcium channel blockers
Dihydropyridines
| Non-dihydropiridines
99
Mechanism of action of dihydropyridines
Act primarily on vasculature —> vasodilation
Week effect on cardiac Ca-channels
—> decrease SVR and contractility
100
Suffix of dihydropyridines
Dipine (amlodipine)
101
What are the two subclasses of non-dihydropyridines ?
Benzothiazepines
| Phenylalkylamines
102
Mechanism of action of non-hydropyridines
Affect cardiac and vascular Ca-channels
| —> decrease HR, contractility and SVR
103
Examples of non-hydropyridines
Az: diltiazem
Ami: verapamil
104
Adverse effects of calcium channel blockers
Dizziness and headache
Flushing, peripheral edema, reflex tachycardia
Bradycardia, hypotension
105
Contraindications of dihydropyridine calcium channel blockers
Conditions worsened by tachycardia
| - severe aortic stenosis
106
Contraindications of non-hydropyridine calcium channel blockers
```
Conduction disorders (Wolff-Parkinson’s-white syndrome, AV block)
Acute CHF
```
Maybe pregnancy
107
Effects of activation of B1 receptors
Increase contraction, HR, renin secretion, BP
108
Effects of B2 receptor activation
Bronchodilation, vasodilation of skeletal muscle arterioles (smooth muscle relaxation)
109
Effects of a2 receptor activation
Vasoconstriction and venoconstriction of non-skeletal muscle vessels (smooth muscle contraction)
110
Suffix off beta blockers
Lol
111
Mechanism of action of beta blockers
Reduce sympathetic activity —>
- decreased HR, contractility, renin secretion —>
- decreased HR and CO
112
What are the different classes of beta blockers ?
Cardioselective B-blockers
Non-cardioselective B-blockers
Mixed a and B-blockers
Partial agonists
113
Location of action of cardioselective B blockers and some examples
Blocks B1 receptors
| Metoprolol, atenolol, bisoprolol
114
Site of action of non-cardioselective B-blockers and examples
Blocks all B receptors
| Propranolol (B1, B2)
115
Examples of mixed a and B blockers
Carvedilol, labetalol (a1, B1, B2)
116
Example of a partial agonist beta blocker
Acebutolol (partial B1 agonist)
117
Adverse effects of Beta blockers
Fatigue (due to increased CO)
Bradycardia
Broncho constriction (B2 blockade)
Rebound hypertension (if abruptly discontinued)
118
Contraindications for Beta blockers
Asthma
Bradycardia or 2nd or 3rd degree heart block
Acute CHF
119
Suffix of alpha 1 blockers
Zosin
120
Mechanism of action of alpha 1 blockers
Decrease vasoconstriction and decrease venoconstriction —>
| Decreased SVR
121
Adverse effect of alpha 1 blockers
Orthostatic hypotension
122
Action of direct vasodilators
Arteriolar vasodilation
Uncertain mechanism
—> decrease SVR
123
Adverse effects of direct vasodilators
Reflex tachycardia
Flushing
Hypotension
Immunological lupus like reaction
124
Central acting a2 agonists suffix
Nidine
125
Action of central acting agents
Inhibit presynaptic release of norepinephrine —>
| Decrease HR, SV and SVR
126
Adverse effects
Sedation (central inhibition of neurotransmitter release
Dry mouth
Orthostatic hypotension
Rebound hypotension
127
What risks increase if hypertension goes untreated ?
```
Morbidity
Coronary artery disease
Heart failure
Stroke
Peripheral vascular resistance
Kidney injury
Vision loss
```
128
What drug shows best evidence as first line treatment of hypertension ?
Thiazides
