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Drug Action I > Block 2 - HTN Physiology > Flashcards

Block 2 - HTN Physiology Flashcards

1
Q

What is HTN?

A

High BP resulting from atherosclerosis that block blood flow in major arteries and create excess pressure on arterial walls

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2
Q

How is systemic arterial pressure measured?

A

Conventional cuff over brachial artery

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3
Q

What is the major cause of first strokes, MIs and heart failures?

A

HTN

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4
Q

What is arteriosclerosis and how does it cause embolism?

A

Thickening of arterial walls → arteries lose elasticity losing ability to constrict or dilate → plaque forms → lumen narrows → pressure builds against walls and plaque breaks off → embolism

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5
Q

What is normal BP?

A

<120/<80

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6
Q

What is elevated BP?

A

120-129/<80

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7
Q

What is HTN stage 1

A

130-139/80-89

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8
Q

What is HTN stage 2?

A

140+/90+

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9
Q

What is HTN crisis?

A

180+/120+

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10
Q

What is primary HTN (essential)? Factors?

A

No known cause
90% of cases
1. Genetics
2. Age
3. Diet
4. Smoking and alcohol
5. Sedentary

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11
Q

What is secondary HTN? How is it treated?

A

Identifiable cause associated with hyperthyroidism, CKD, tumors of adrenal gland

Remove underlying cause

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12
Q

What are the factors that affect? Figure

A
  1. Hormones: RAAS, plasma adiponectin (reduce HTN)
  2. Nervous system
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13
Q

How does HTN affect the RAAS?

A

Disruptions of the RAAS → heightens presence of angiotensin II

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14
Q

What is angiotensin? How is important in maintaining HTN?

A
  1. Potent vasoconstrictor
  2. Affects growth and maturation of adipocytes

Adipocytes → cardioprotective adiponectin → regulates energy balance, anti-inflammatory, and anti-plaque → decreasing risk for HTN

Low adiponectin levels in HTN

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15
Q

What does obesity lead to?

A
  1. Increased angiotensin II in adipocytes of visceral fat
  2. Reduced plasma levels of adiopectin
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16
Q

What is endothelial dysfunction? Risk factors?

A

Dysfunction in endothelium that regulates BP of vasoactivity (dilators: NO)

Reduced amount of NO from smoking, aging, HTN

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17
Q

How is the sympathetics NS affected in HTN?

A
  1. Increased in HTN
  2. Increased HR, blood flow, renal retention of Na+
  3. NE raises BP
  4. E promotes vasoconstriction
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18
Q

How can alcohol consumption contribute to HTN?

A
  1. Activates RAAS → increased renin and angiotensin II
  2. Vasoconstriction → depletes NO
  3. Activates SNS
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19
Q

How can lifestyle factors contribute to HTN?

A
  1. Increased stress
  2. High salt intake
  3. Lack of PE
  4. Obesity
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20
Q

How can genetics contribute to HTN?

A
  1. Increased in E and NE seen in a family history of HTN
  2. African Americans have the highest rate of HTN
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21
Q

What are the clinical manifestation of HTN?

A
  1. Asymptomatic → damage is progressively occurring
  2. Symptoms are rare until BP is really high (DZ, nosebleeds, HA, facial flushing, blood spots in eyes)
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22
Q

What are the long term consequences of HTN?

A
  1. MI
  2. Stroke
  3. CKD
  4. Vision loss
  5. ED
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23
Q

What is the difference between HTN crisis and urgency?

A

Crisis: Organ damage in CV, kidneys, and brain (aggressive. immediate treatment)
Urgency: No organ damage

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24
Q

What are the signs of severe HTN?

A
  1. Retinal hemorrhage
  2. Papilledema (edema in retina)
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25
Q

Signs and symptoms of HTN?

A
  1. Dyspnea
  2. Acute LHF
  3. Diminished renal function
  4. Stroke
  5. HTN encephalopathy (leaky brain capillaries, seizures, paralysis, coma, HA)
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26
Q

What are the secondary causes of HTN crisis?

A
  1. Pheochromocytoma
  2. Cocaine use
  3. Preeclampsia and eclampsia
  4. Acute aortic dissection
  5. Renovascular HTN
  6. Hyperthyroidism (thyroid storm)
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27
Q

What is pheochromocytoma? Etiology?

A

tumor of chromatin tissue in the adrenal medulla
Rare

Sympathetic nerve cells release catecholamines→ vasoconstriction → HTN

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28
Q

Clinical manifestations of pheochromocytoma?

A
  1. Paroxysmal (periodic episodes)
  2. Whole body: flushing, HBP, sweating, DZ, fatigue
  3. Heart: tachycardia
  4. Marked variability in BP between episodes
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29
Q

Pheochromocytoma diagnosis? Why do we use each method?

A
  1. Measure urinary catecholamines
  2. Measure plasma catecholamines
  3. MRI and CT to locate tumor
  4. Radioisotopes (localize chromatin tissue)
  5. Surgical endoscopic removal
  6. Drugs that block the actions or synthesis or catecholamines
30
Q

How can cocaine cause HTN?

A
  1. Strong stimulant
  2. Inhibits NE reuptake in sympathetic neurons → vasoconstriction → BP and HR → Heart is overworked and blood vessels weaken
31
Q

What are the dangers of chronic cocaine use?

A

Increased risk of an aneurysm → internal bleeding

32
Q

What are the clinical manifestations of cocaine induced HTN?

A
  1. Chest pain
  2. aneurysm
  3. myocarditis
  4. Cardiomypothy
  5. Arrhytmias
  6. Stroke
  7. CV events
33
Q

How does pregnancy cause HTN?

A

Increased renin, angiotensin I and II, estrogen, progesterone, prolactin, aldosterone → alter vascular activity

Complicates 5-10% pregnancies

34
Q

How is BP effected in each trimester of pregnancy?

A
  1. BP normally decreases (CV increases, PVR decreases)
  2. BP continues to decrease to low point
  3. BP gradually rises
35
Q

What is preeclampsia?

A

Pregnancy specific syndrome with maternal and fetal manifestations
1. Elevation of BP (>140/>90)
2. Proteinurea (20 weeks of gestation, ≥300 mg/day)

36
Q

What is the diagnosis of preeclampsia?

A
  1. ≥160/≥110
  2. Proteinuria (>2g/day)
  3. Serum creatine (>1.2 mg/dL)
  4. Platelet count (<100,000cells/m^3)
  5. Elevated ALT and AST
  6. HA, visual disturbances
  7. epigastric pain
  8. HELLP
37
Q

What is HELLP?

A

Symptoms of preeclampsia
Hemolysis, elevated liver enzymes, low platelet count

38
Q

What is the probability of contracting preeclampsia?

A
  1. Primarily during first pregnancy
  2. Hydatidiform mole
  3. increased risk of preeclampsia for chronic HTN
39
Q

What is hydatidiform mole?

A

Abnormal pregnancy caused by a pathologic ovum → mass of cysts

40
Q

What is etiology of preeclampsia?

A

Placenta is the key factor
1. Decrease in placental blood flow leads to release of toxic mediators that alter endothelial cells in BV in kidney, brain, liver, heart
2. Cure is delivery

41
Q

How does renal change due to preeclampsia?

A
  1. Decreased GFR and RBF
  2. Impaired Na+ excretion
  3. Edema
42
Q

How does liver damage change due to preeclampsia?

A
  1. HELLP syndrome from hepatocellular necrosis with elevated liver enzymes
  2. elevated LFTs
43
Q

What is the mechanism of braking?

A
  1. Activation of sympathetic nervous system
  2. Activation of RAAS
  3. Decreased arterial BP, renal epithelial cell hypertrophy
  4. Increased renal epithelial transporter expression and alterations in natriuretic hormone (ANP)
44
Q

What is the most common hematologic complication of preeclampsia? What is it?

A

Thrombocytopenia is caused by platelet deposition at site of endothelial injury

45
Q

What are the outcomes of women contracting preeclampsia?

A
  1. More sensitive vasoconstrictor activity of the RAAS
  2. More responsive to other vasoconstrictors
  3. Prostacyclin-thromboxine imbalances
  4. Insulin resistance
46
Q

What is prostacyclin and thromboxane?

A

Vasodilator and constrictor

47
Q

What are the fetal effects of preeclampsia?

A

Decreased placental blood flow in intrauterine growth restriction (IGR) → infants who are small for gestational age

48
Q

How does eclampsia differ from pre?

A

Consulsive stage that attributes to increased blood coagulability and fibrin deposition in cerebral blood vessels

49
Q

What is the treatment for preeclampsia and eclampsia?

A
  1. Delivery
  2. Bed rest
  3. Anti-HTN (ACEIs may cause injury in 2nf and 3rd tri)
50
Q

What is acute aortic dissection?

A

Hemorrhage into vessel wall with longitudinal tearing of the vessel wall to form blood filled channel → transverse tear in the intimacy and internal media

51
Q

What is the etiology of acute aortic dissection?

A

Weakened or degenerative changes in the eleastic changes in the elastic and smooth muscle layers (40-60 YO more male than female)

52
Q

What are the risk factors of acute aortic dissection?

A
  1. HTN
  2. Degeneration of medial layer of vessel wall
  3. Connective tissue disease
  4. Pregnancy
  5. Congenital defects of aortic valves
  6. Cardiac surgery
  7. Aortic coarctation
53
Q

What are the levels of dissection?

A

A and B

54
Q

What is dissection type A?

A
  1. Involve the ascending aorta only or both descending and ascending
  2. May cause closure of aortic valve
  3. Risk of aortic rupture → blood moving to pericardium compressing heart
55
Q

What is dissection type B?

A

Doesn’t involve ascending aorta

56
Q

What are the classes of aortic dissection?

A
  1. Level of dissection
  2. Time of onset
57
Q

What are the classifications of dissection based on time of onset?

A

Acute and chronic (persistence of dissection flap or channel)

58
Q

Dissection symptoms of ascending and descending aorta?

A

A: pain in anterior chest
D: Pain in back

59
Q

Early stages of dissection?

A

BP is moderately or markedly elevated

60
Q

Advanced stage of dissection?

A

BP and pulse in unobtainable in one or both arms → disrupts arterial flow to arms

61
Q

How does renovadcular HTN occur?

A

Renal blood flow becomes disrupted

62
Q

What are common etiologies of renovasc HTN?

A
  1. Atherosclerosis: plaque builds up and block BF
  2. Fibromuscular dysplasia: muscle and tissue thicken on the artery wall and harden into rings → block BF
  3. Rena artery stenosis: narrowing of kidney arteries
  4. Structural problems: birth

RAAS is activates → BP elevates

63
Q

How does stenosis increased BP?

A
64
Q

Clinical manifestation of renovascular HTN?

A
  1. Typically asymptomatic
  2. Can present with:
    - High blood pressure (can be hard to control)
    - Pain in the back or side
    - Blood in urine
    - Breathing problems from fluid buildup in the lungs
    - Weight gain
    - Fluid buildup in legs, ankles, or feet
65
Q

How can HTYD (thyroid storm) → HTN? Figure

A

Marked by extreme overproduction of T3 and T4 by the thyroid gland

66
Q

Clinical manifestation of thyroid storm?

A

Similar to HTHYM but more sudden
Tachycardia: 140 bpm
A fib
High fever
Persistent sweat

67
Q

What is white coat HTN?

A

Artificially HBP reading because patient experiences fight-or-flight symptoms around med workers

68
Q

How do you diagnose HTN?

A

Measurement of BP (inflatable cuff and pressure measuring gauge)

69
Q

What are the nonpharm of HTN?

A

TLC:
1. Restrict Na+ consumption
2. Limit alcohol
3. Stop smoking
4. Maintain optimal weight
5. Reduce fat
6. Reduce stress
7. Increase PA

70
Q

What are the first-line AHTN?

A
  1. Angiotensin converting enzyme inhibitors (-pril, ACE)
  2. Angiotensin receptor blockers (-sartan, ARBs)
  3. Calcium channel blockers (CCBs)
  4. Thiazide diuretics
71
Q

What are the second line AHTN?

A
  1. Adrenergic blockers
  2. Centrally acting drugs
  3. Direct acting vasodilators
  4. Direct renin inhibits
72
Q

Identify the MOA of antihypertensives?

A

Drug Action I (32 decks)

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