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Med 411 > Week 9 HTN > Flashcards

Week 9 HTN Flashcards

1
Q

What are the 3 layers of blood vessels?

A

Tunica intima - endothelium, basement membrane, subendothelial CT
Tunica media - Smooth mm that secrete elastin fibers, CT w/collagen and elastin
Tunica adventitia - Loose CT, fibroblasts, nerves, vasa vasorum

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2
Q

Discuss the vascular endothelium

A

Simple squamous cells that line blood vessels and align with direction of blood flow.
Luminal surfaces express receptor and adhesion molecules important for immune response.

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3
Q

What are the 3 types of arteries?

A
  1. Large (elastic) arteries - closest to heart, thick media with elastic laminae, high pressure.
  2. Medium (muscular) arteries - distributing artieres to organs (named), thick media with lots of sm mm.
  3. Arterioles - Smallest arteries regulating blood flow to caps, regulate BP, thin media with 1-3 layers of sm. mm.
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4
Q

Elastic laminae

A

Elastin secreted by sm. mm forms elastic fibers which come together to form sheets of elastin.

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5
Q

What are the key features of arterial walls?

A

Thick vessel wall compared to size of lumen.
Tunica media is the most prominent layer.
Large arteries have elastic laminaie
Medium arteries have elastic fibers.
Tunica adventitia is the same size as the tunica media.

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6
Q

What are the three types of capillaries?

A
  1. Continuous - endothelial cells with tight junctions, pericytes, found in lung, brain, thymus, muscle.
  2. Fenestrated - endothelial cells with fenestrations to allow movement of fluid and sm. molecules, less pericytes, found in endocrine glands, kidney, intestines.
  3. Discontinuous or Sinusoids - large, irregularly shaped endothelial cells with gaps, found in liver, spleen, bone marrow.
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7
Q

What are the 3 types of veins?

A
  1. Large veins - largest but thin walls, large lumen, high capacitance, holds 70% of the blood volume.
  2. Medium veins - conducts blood from tissues, thing walls, large lumen, valves, thick adventitia w/sm. longitudinal mm and vaso vasorum, travel with medium arteries.
  3. Venules - receive from caps, thin walls, collapsed lumen, valves, travel with arterioles.
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8
Q

What are the key features of veinous walls?

A

Thin, distensible lumen, lumen often collapsed.
Think media.
Thick adventitia.
Valves.

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9
Q

What are the ways blood gets back to the heart?

A

Muscle pump
Respiratory pump
Venoconstriction (sympathetic tone)

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10
Q

What are the functions of the lymphatic system?

A

Return of excess fluid and protein.
Immune defense.
Transport of absorbed fat.

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11
Q

How does flow relate to pressure and resistance?

A

Flow is proportional to pressure and inversely proportional to resistance.
Pressure goes up = flow goes up
Resistance goes up = flow goes down. This relationship is exponential.

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12
Q

What is the most effective way to alter flow in the arterial system?

A

Increase or decrease the radius of the arteries.

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13
Q

What are the 2 overarching controls for blood pressure?

A

Neural (ANS)
Humoral (endocrine/renal)
These feedback loops work together.

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14
Q

How does the autonomic nervous system control BP?

A
  1. Vasoconstriction or vasodilation - vasomotor tone determines peripheral vascular resistance.
  2. Alter CO - CO=HRxSV BP=COxSVR
  3. Change the volume of blood in circulation - vasoconstriction shifts blood from venous system to the R heart and increases preload which results in increased CO.
    These mechanisms are SHORT TERM.
  4. RAAS & NPs changes blood volume.
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15
Q

How do the humoral controls affect BP?

A

Regulation of blood volume through Na and H2O via feedback loops in the hypothalamus, pituitary gland, adrenal cortex, and kidneys.

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16
Q

What is an additional way BP is altered?

A

Arterial elasticity (compliance)
Can be functional or structural in origin.
Functional - determined by the degree of activity.
Structural - determined by the disruption of elastin, collagen deposition, and altered extra-cellular matrix.

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17
Q

What is the pre-ganglionic neurotransmitter for both divisions of the autonomic nervous system?

A

Acetylcholine.

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18
Q

What is the post-ganglionic neurotransmitter for the sympathetic nerve terminals?

A

Norepinephrine

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19
Q

What is the post-ganglionic neurotransmitter for the parasympathetic nerve terminals?

A

Acetylcholine

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20
Q

Thoracolumbar outflow

A

T12-L2
SNS
Pre-ganglionic fibres leave spinal cord with motor nerves then branch off through white rami communicantes to the sympathetic trunk alongside the spinal column as paravertebral ganglia.
Post-ganglionic fibres that originate in ganglia, leave through gray rami communicantes and meet up with the spinal nerve.

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21
Q

How does venous constriction affect blood pressure?

A

Increased venous return to R atrium.
Increased end diastolic volume.
Increased force of ventricular contraction (stroke volume)
Overall increased CO.
Rapid result.

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22
Q

Craniosacral outflow

A

CNI-XII
S1-S5
Vagus nerve (CNX) relates to cardiovascular system.

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23
Q

Baroreceptor reflex

A

Baroreceptors in carotid sinus and aortic arch.
Via CN IX (glossopharyngeal) and CN X (vagus nerve) to the posterolateral medulla and pons.
Posterolateral medulla and pons send signals to vasoconstrictor and vasodilator centres.
Results in decreased SNS outflow in response to increased blood pressure.
Negative feedback loop.

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24
Q

ANP & BNP

A

Released by atrial myocytes, ventricles in response to stretch, Ang II, endothelin, and SNS activity.
Venodilation.
Decreased central venous pressure (CVP).
Decreased venous return to RA.
Decreased CO.
Arterial dilation.
Decreased peripheral resistance.
Vasodilation is via increased cGMP
Increased GFR
Decrease renin release.
Net result is decreased BP

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25
Q

Local regulation of blood flow.

A

Regulated by metabolic requirements.
Vasodilation caused by increased:
PCO2
Lactic acid
H+
K+
Adenosine
ADP
Histamine
Bradykinin
Prostacyclin
Endothelial derived NO

Vasoconstriction caused by decreased:
PO2
5-HT (serotonin)
Endothelin

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26
Q

Nitric Oxide

A

Released from endothelial cells in response to shear stress, Ach, serotonin, bradykinin, thrombin.
Activates GC which converts GTP to cGMP and activates cGMP-dependent kinase.
Effect only lasts seconds.

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27
Q

Autoregulation

A

Despite fluctuations in BP, blood flow to most tissues is maintained at a relatively constant rate.

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28
Q

What 2 theories explain autoregulation?

A

Metabolic theory: Factors causing vasodilation get “washed out” leading to vasoconstriction.
Mygenic theory: Stretch of vessel walls causes contraction of smooth mm.

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29
Q

What areas does autoregulation not apply to and how are they regulated?

A

Brain: Increase PaCO2 and H+ cause vasodilation, increasing cerebral blood flow.
Kidneys: Increase in NaCl leads macula densa to release ATP which is converted to adenosine, leading to Ca release, vasoctx of afferent arteriole, decrease secretion of renin.

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30
Q

When do symptoms of hypertension begin to develop?

A

Only when there is advanced damage in the target organs (brain, eyes, heart, kidneys).

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31
Q

What is diagnosis of HTN based on?

A

Solely on accurate measurement of BP.

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32
Q

How does HTN affect target organs?

A

Simulates vascular remodeling
Accelerates atherosclerosis
These lead to increased peripheral vascular resistance and reduced flow to tissues.

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33
Q

What is the most common type of hypertension?

A

Primary (95%)
Secondary (5%)

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34
Q

How is treatment of hypertension determined?

A

Tailored to the patient based on age, frailty, lifestyle factors, and co-morbidities.

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35
Q

True hypertensive emergencies

A

Uncommon. Severely elevated BP with TOD.
Includes:
Encephalopathy; headache, vomiting, confusion, seizures, coma
Intracranial hemorrhage
Angina pectoris; increased afterload leads to increase work and O2 consumption
Impaired LV contractility leads to cardiogenic pulmonary edema
Aortic coarctation
Ischemic stroke
Acute kidney injury; delirium, pericardial effusion, edema, hyperkalemia, acidosis, increased creatinine, nitogen, urea.
Marked BP elevation post transplant and some surgeries.
Treating very high BP in other situations is unwarranted and can be harmful.

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36
Q

Epidemiology of HTN

A

Prevalence doubled btwn 1990-2021 in low and middle-income regions.
Prevalence decreased in high-income countries.
1/4 Canadians age 20-79.
M>W.
Risk at 60 years of age is 50%.
Lifetime risk for newcomers is 90%.

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37
Q

What factors are associated with HTN?

A

Obesity
Reduced fruit and veg intake
Lower levels of exercise
Diabetes
Chronic kidney disease

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38
Q

What percentage of HTN patients have their BP controlled (<140/90)?

A

Only 2/3.
Adequate treatment in Canada seems to be waning.

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39
Q

What is considered the major culprit in HTN?

A

High sodium content in processed foods.

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40
Q

HTN and CV risk

A

CV disease is 2nd leading cause of death in BC.
MI, stroke, peripheral vascular disease.
HTN accelerates atherosclerosis, increasing the risk of CV disease.
HTN patients often have other CV risk factors (obesity, T2D, dyslipidemia)

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41
Q

What levels of BP reduction are associated with reduced risk of MI and stroke in those under 60 years of age?

A

Lower 10-15 mmHg systolic
Lower 5-6 mmHg diastolic

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42
Q

NNT (50 year old males)

A

120 for 5 years to prevent 1 death.

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43
Q

Gold standard for diagnosis of HTN

A

Hypertension Canada’s guidelines.
Mean office BP: >180/110
OBPM: >140/90 averaged across 3 separate readings at least one week apart.
AOBP/ABPM/HBPM: >135/85
Diabetes OBPM >130/80 for 3 or more separate readings on different days.

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44
Q

Primary HTN

A

HTN diagnosis with no obvious causes to explain it.
Likely multifactorial.
Mosaic theory of HTN involves intersection of genetic, environmental, adaptive, neural, mechanical, and hormonal factors.
Likely genetic factors.
Genes identified that code for the subunits on tubular Na channels - leads to increased Na retention.

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45
Q

What component of the RAAS is indicated in vascular remodelling?

A

Angiotension II.

46
Q

How does immune activation in the kidneys affect BP?

A

Immune activation leads to release of cytokines, which cause vasoctx, further increasing peripheral vascular resistance.

47
Q

Metabolic syndrome

A

HTN + Dyslipidemia + T2D
Net effect is activation of RAAS, capillary basement membrane thickening in kidneys, endothelial and vascular smooth mm dysfunction, vascular remodelling, atherosclerosis.

48
Q

When should secondary HTN be considered?

A

Extremes of age with unexpected target organ damage.
Abrupt onset.
Atypical response to therapy.
Association with kidney disease.
Hypokalemia or hypercalcemia.

49
Q

Approach to secondary HTN.

A

A: Accuracy, sleep Apnea, primary Aldosteronism
B: Bruits, Bad kidneys
C: Catecholamines secreted by adrenal medullary tumors (pheochromocytoma), Coarctation of aorta, Cushing’s syndrom
D: Diet, Drugs (Rx or non-Rx including alcohol)
E: Erythropoetin, Endocrine disorders

50
Q

Target organ damage manifests where?

A

Eyes (retinopathy)
Brain (cerebrovascular disease)
Heart (hypertensive heart and coronary artery disease)
Kidneys (hypertensive nephrosclerosis)

51
Q

Hypertensive retinopathy

A

Retinal vessels go through sequential changes.
Hard exudates
Flame-shaped hemorrhages
Dot & blot hemorrhages
Papilledema
Grades 1-4.
Grade 1: diffuse arterial spasm and narrowing, leads to fibrosis, leads to focal narrowing.
Grade 2: Aterio-venous nicking d/t arteriole wall thickening, compressing where a vein crosses the artery.
Assessment done with ophthalmoscope directed at the fundus.

52
Q

HTN and stroke

A

Stroke is the 3rd most common cause of death in N. America.
HTN is the number 1 risk factor for stroke.
Ea 2-3 mmHG decrease in systolic could reduce incidence of stroke by 10%.

53
Q

Hypertensive Heart Disease

A

Arterial HTN causes increased after load on heart.
Leads to left ventricular hypertrophy (LVH).
LVH diagnosed w/ECG, CXR, echocardiogram, physical exam.
LVH leads to hemodynamic stress, leads to decompensated heart failure.
S&S: shortness of breath, orthopnea, leg edema.

54
Q

Hypertensive Kidney Disease

A

HTN is the second leading cause of chronic kidney disease (second to diabetes).
Chronic changes from vascular injury - autoregulation no longer effective.
Arterioles thicken - reduction in lumen, loss of flow (rarefaction).
Net effect is increased vascular resistance and parenchymal scarring.
Results in bad filtration, reabsorption, excretion.
Albumin from blood spills over into urine (microalbuminuria)

55
Q

Which two signs, each on it’s own merit, are predictors for adverse cardiovascular events?

A

LVH
Microalbuminuria

56
Q

What is the general range of BP that is associated with hypertensive emergencies?

A

250/140.

57
Q

Classes of HTN drugs

A
  1. Diuretic agents
  2. RAAS inhibitors
  3. Ca channel blockers
  4. Adrenergic receptor antagonists
  5. Direct vasodilators
  6. Central-acting agents.
58
Q

Major classes of Diuretic agents

A
  1. Thiazides
  2. Loop diuretics
  3. K-sparing diruetics
59
Q

Classes of RAAS inhibitors

A
  1. ACE inhibitors
  2. Angiotensin II receptor blockers
  3. Renin inhibitors
  4. Aldosterone receptor antagonists
60
Q

ACE inhibitors

A

“pril”
Block conversion of Ang I - Ang II.
Block the breakdown of bradykinin - cough.
Results:
Inhibits vasoctx
Inhibits aldosterone secretion
Inhibits NaCl reabsorption
Increased vasodilation (d/t bradykinin)
Overall effects: decreased SVR/decreased preload

61
Q

Common/important adverse effects of ACE inhibitors

A

Cough (d/t bradykinin)
Hyperkalemia (d/t reduced aldosterone)
Renal dysfunction (if decreased renal blood flow)
Hypotension
Angioedema (rare)

62
Q

ACE inhibitors are contraindicated for?

A

Pregnancy: teratogenicity and increased complications.
Renal artery stenosis.

63
Q

Angiotensin II receptor blockers (ARBs)

A

“sartan”
Angiotensin II antagonists
Overall effects: decreased SVR/decreased preload

Allow for breakdown of bradykinin - no cough.

64
Q

Common/important adverse effects of ARBs

A

Dizziness
Hypotension
Hyperkalemia (reduced aldosterone)
Renal dysfunction (if decreased renal blood flow)

65
Q

When are ARBs contraindicated?

A

Pregnancy

66
Q

Renin inhibitors

A

“ren” (only 1 drug in this class, aliskiren)
Block conversion of Ang to Ang I.
Similar effects to ARBs.
Adverse effect is diarrhea.
Contrainticated in pregnancy.

67
Q

Calcium channel blockers (CCBs)

A

Dihydropyridines (DHPs) “dipine”
Act as vasodilators

Non-dihydropyridines
Benzothiazepines “tiaz”
Phenylalkylamines “amil”
Act primarily on Ca channels in the heart.

Decrease vascular sm mm ctx (decrease SVR)
Decrease cardiac conduction and contractility (decrease HR and CO)
Blocks the Ca signal to adrenal cortex to release aldosterone.

68
Q

Common/important adverse effects of CCBs

A

Vasodilatory effects: Flushing, peripheral edema, reflex tachycardia.

Cardiac effects: Bradycardia, hypotension.

Dizzyness, headache.

69
Q

When are CCBs contraindicated?

A

Conditions that are worsened by or do not tolerate tachycardia (severe aortic stenosis)
Non-DHPs: cardiac conduction disorders.

70
Q

CCBs and pregnancy

A

Not enough data to rule out risk.
Nifedipine is recommended for use in pregnancy.

71
Q

Adrenergic receptor antagonists

A

Beta-blockers
Alpha-1 blockers

72
Q

Beta blockers

A

“lol”
Cardio selective B-blockers only block B1 receptors (metoprolol, atenolol, bisoprolol)
Non-cardioselective B-blockers block B1/B2 receptors (propranolol)
Mixed a/B-blockers block a1, B1/2 receptors (carvedilol, labetalol)
Partial agonists have some B1 activity (acebutolol)

73
Q

Common/important adverse effects of beta blockers

A

Fatigue (d/t decreased CO)
Bradycarcia
Bronchoconstriction (except cardio selective)
Rebound hypertension (if abruptly discontinued)

74
Q

Contraindications for beta blockers

A

Asthma
Bradycarcia
2nd or 3rd degree AB block
Acute congestive heart failure.

75
Q

Beta blockers and pregnancy

A

Labetalol is considered safe during pregnancy.
Society and OBGyn Canada lists labetalol, acebutolol, metoprolol, pindolol, propranolol for tx of HTN in pregnancy.

76
Q

Alpha-1 antagonists

A

“zosin”
Decrease vasoconstriction of arteries and arterioles.
Decrease venoconstriction.
Overall effect is decreased SVR.
Most common side effect is orthostatic hypertension.

77
Q

Direct vasodilators

A

Cause arteriole vasodilation.
Hydralzaine: inhibits Ca release in Sarcoplasmic recticulum of arterial smooth mm.
Decreases SVR.
Adverse effects: reflex tachycardia, flushing, hypotension, mimic of lupus.
Not commonly used for HTN except in pregnancy or HTN crisis.

78
Q

Central-acting agents

A

A2 agonists
Inhibits release of norepi.
Overall effect: Decrease HR, SV, SVR
Adverse effects: sedation, dry mouth, orthostatic hypotension, rebound hypotension.
Risks during pregnancy depend on the individual drug; methyldopa considered safe.
Clonidine effects are unknown.

79
Q

Treatment protocol

A

Non-pharmacologic interventions should be started first.
Isolated primary moderate to severe HTN: low-dose thiazide diuretics. ACE inhibitors and CCBs don’t show the same high-quality evidence. High dose thiazides were less beneficial.

80
Q

Discuss accurate HBPM

A

7 day (dn have to be consecutive days) duplicate readings morning and after supper before medications.
Take an average of all but the first day.
Minimum 12 readings.

81
Q

Masked HTN

A

Normal in office but increases at work or at night when sleeping and not measured.
Most dangerous type.
More common in younger pts and in men.
Higher CV disease risk than patients with sustained HTN.
Suspect if target organ damage or LVH.

82
Q

Normotension

A

True normal values for OBPM

83
Q

White coat HTN

A

Only high in office but 24hr ABPM are not elevated.
Occurs in 20-30% of people labellesd with HTN.
Still have higher risk for CV and all cause mortality than normal.

Suspect if patients d/n have target organ damage, report out of office readings that are lower, feel lightheaded/dizzy w/meds, more common in elderly women.

Also watch out for people that only report 120/80 readings and disregard all other high readings.

84
Q

When should children be checked for HTN?

A

Age 3 and up.

85
Q

Tests for TOD with hypertensive emergency

A

Heart Failure: Shortness of breath, volume overload. CXR, BNP
Coronary syndrome/angina: Chest pain. ECG, troponin.
Stroke/Encephalopahy: Unilateral weakness/confusion. CT head.
Aortic dissection: Tearing chest pain radiating to back. CT angiogram.
Renal failure: Decreased urine output. Creatinine, urinalysis.
Malignant hypertension: Blurred vision, confusion, papilledema. Fundoscopic exam, MRI brain.

86
Q

Hypertensive Urgency

A

Severely elevated BP without TOD.
Usually managed in ER.
Investigate for TOD.
Target is to lower BP by 25% over hours or over the day.
Treated with oral medications such as their own medications.
Short acting medications oral captopril, oral lasix, oral clonidine.

87
Q

Routine investigations for all HTN

A

Screen for substances that exacerbate blood pressure.
TOD
Cardiac risk factors
Secondary screen cause
Pregnancy test

88
Q

Secondary HTN screenings

A

OSA: obese, symptoms of OSA, resistant hypertension.
Renal disease: All
Renovascular disease: Young women (FMD), flash pulmonary edema, worsening kidney function, resistant HTN
Primary Aldosteronism: resistant HTN, low K+, family hx.
Pheocromocytoma/Cushings: Only if S&S
Thyroid/Parathyroid: Routinely screened by age
Coarctation of Aorta: Asymmetric BP in each arm.

89
Q

Screening tests for OSA

A

STOP-BANG
Overnight polysomnography

90
Q

What is the most common reason for family doctor visits?
What is the patients #1 concern?

A

HTN
What can they do that does not involve meds?

91
Q

Based on twin studies, what amount of blood pressure variation is thought to be due to genetics?

A

30-60%

92
Q

Can lifestyle modifications be beneficial in those with high genetic risk for HTN?

A

Yes!!

93
Q

Lifestyle factors for uncomplicated HTN

A

Age
Obesity and insulin resistance
High Na diet
Low K diet
Sedentariness
Poor sleep
Stress

94
Q

How does aging pose a risk for HTN?

A

Distensibility decreases with age.
Elastin is replaced by Type 4 collagen (steel)
Widens difference between systolic and diastolic.
Systolic increases with age, but after mid 50s diastolic plateaus or decreases causing isolated systolic hypertension.

95
Q

How do obesity and insulin resistance contribute to HTN?

A

SNS activation: Increased plasma volume and CO
RAAS activation
Shifting of pressure naturesis to a higher BP threshold in obesity.

96
Q

What is the link between screen time and HTN?

A

> 4 hours/day is associated with hyperinsulinemia even in those physically active (active couch potato).
Chronic unbroken periods of muscular unloading suppresses lipoprotein lipase activity and reduced glucose uptake.

97
Q

What is the Hypertension Canada RDA for sodium?

A

2 g/day

98
Q

Salt sensitivity.

A

Extent of BP change after abrupt changes in salt intake.
Increases with age, more marked in African decent.
Activation of endothelial Na channels that impair NO vasodilation.
Increases with aging (>40).

99
Q

What is the relationship between potassium and blood pressure?

A

Inversely related.

100
Q

Effects of alcohol on BP

A

> 2 drinks/day = 1/5-2 x increase in HTN compared to non-drinkers.
Dose related, especially when intake >5/day.
Binge drinking counts.
Stimultes SNS, RAAS, increases cortisol, inhibits NO.

101
Q

Effects of poor sleep on BP

A

SNS hyperactivity resulting in nocturnal HTN.
Frequent daytime napping is associated with 12% increased risk of developing high BP

102
Q

Stress and BP

A

High imbalance: high effort and low reward = stress
High overcommitment not related with increased BP.
Work HTN is called MASKED HTN

103
Q

What substances contribute to high BP?

A

Simulants
Decongestants
Prednisone
Some tricyclic antidepressants
NSAIDs
Suppliements: St. John’s Wort, Ephedra, Ginko, Ginseng

104
Q

Lifestyle recommendations for all HTN pts.

A
  1. Excercise
  2. Weight reduction to health BMI
  3. Alcohol consumption
  4. Diet - DASH
  5. Sodium reduction
  6. Stress managment
105
Q

What are the screening tools for alcohol use disorder?

A

CAGE
AUDIT

106
Q

What causes withdrawal symptoms in alcohol use disorder?

A

When dependent, tolerance occurs as GABA receptors are desensitized and Glutamate is upregulated.
Quitting cold turkey - increased Glutamate causes seizures.
Gets worse with each withdrawal episode.

107
Q

Complicated withdrawal

A

More symptoms
Increased HR
Increased BP
headache
Seizures - usually w/in 6-48 hours after cessation, can happen for 72 hours. 3% will progress to epileptic status. Tx is BENZOs.
Hallucinosis - transient benign hallucinations, they know they are hallucinating, distinct from DT.
Delirium Tremens - Significant autonomic activity, tachy, HTN, hypothermic, disturbance of consciousness, usually occurs day 3 and resolved in 1-5 days.

108
Q

Benzos for withdrawal

A

Short acting used for elderly or those with liver disease (lorazepam/oxazepam)
Long acting for everybody else (Diazepam, chlordiazepoxide)
Also NRT for nicotine withdrawal as this can increase the CIWAS score.
Benzo taper is informed by PAWSS.

109
Q

Assessment tools for alcohol withdrawal

A

CIWA-Ar Clinical Institute Withdrawal Assessment - Alcohol revised: Gold standard, Indicates benzo use and AWD severity.

PAWSS Prediction of alcohol withdrawal severity score: Assesses for low-risk (outpatient) vs high-risk (inpatient).

110
Q

What medications are given for alcohol use disorder?

A

Naltrexone: can start while using alcohol. 1/day. Opioid receptor blocker, decreases dopamine. Can affect liver, need normal liver function. Cannot use opioids when using.

Acamprosate: can start while using alcohol. 3/day. Can cause renal impairment. Not safe for breast feeding.

Topirimate
Gabapentin

111
Q

Psychosocial interventions for alcohol use disorder

A

Peer based supports: AA, SMART
Recovery based treatment programs: Counselling, CBT, MI, MET, DBT. Day tox. Intensive bed treatments.

Med 411 (6 decks)

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