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SRNAAnatomy II > Hypertension > Flashcards

Hypertension Flashcards

1
Q

– Primary HTN (essential)

A

cause is unknown (~90% of cases)

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2
Q

– Secondary HTN

A

has definable cause (less common)

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3
Q

Normal Blood pressure

A

SBP Less than 120

DBP less than 80

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4
Q

Pre HTN

A

SBP 120-139

DBP 80-89

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5
Q

Stage I HTN

A

SBP 140-159

DBP 90-99

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6
Q

Stage II HTN

A

SBP >160

DBP > 90

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7
Q

Hypertensive Crisis

A

SBP >180

DBP>110

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8
Q

B2 receptors on PVR

A

Decreases

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9
Q

Local regulators: Nitrous oxide on PVR

A

Decreases

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10
Q

Local regulators: Adenosine on PVR

A

Decreases

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11
Q

Local regulators: Prostaglandins on PVR

A

Decreases

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12
Q

No matter how high the C.O. or TPR,

A

renal excretion has capacity to completely return BP to normal via reducing intravascular volume

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13
Q

Pressure natriuresis:

A

normal kidney response to INCREASING BP = INCREASING urine volume and Na+ excretion
This is blunted in hypertensive pts:
– Microvascular and tubulointerstitial injury in kidney secondary to HTN impairs Na+ secretion

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14
Q

Baroreceptor Reflex:

A

Changes in BP detected by stretch receptors (baroreceptors), located in large arteries above heart
– aortic arch
– aortic sinuses (behind aortic valve cusps)
– carotid sinus (base of each internal carotid artery)

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15
Q 
Essential HTN
\_\_\_\_\_\_\_of cases, exact cause \_\_\_\_\_\_
• Dx’d after \_\_\_\_\_\_\_\_\_\_
• Thought to result from \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_with environmental stressors.
• The defects may be \_\_\_\_\_\_\_\_\_\_\_\_
A

90% of cases, exact cause unknown.
• Dx’d after rule out Secondary HTN.
• Thought to result from multiple defects in pressure
regulation that interact with environmental
stressors.
• The defects may be acquired or genetic.

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16
Q

HTN Abnormalities

A

Heart, Blood Vessels & Kidney

Also contribute to development HTN.

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17
Q

HTN and heart

A

HEART

– Increased C.O. – HTN pts. have excessive sympathetic response under psychologically stressful conditions.

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18
Q

HTN and Blood Vessels

A

Increase TPR secondary to to Increase sympathetic activity
– abnormal tone secondary to local factors (ex. endothelin)
– ion channel defects in smooth muscle

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19
Q

KIDNEY causes (FII)

A

causes volume based HTN via excess Na+ & H20 retention:
- fails to regulate renal blood flow
- ion channel defects that increase Na+ retention
– inappropriate renin excretion
(Renin secretion should be suppressed by high blood pressure, so even “normal” levels are inappropriate in HTN pts.

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20
Q

ESSENTIAL HTN : Other genetic factors (IOM)

A

Other genetically linked factors:
– Insulin resistance/DM
– Obesity
– Metabolic Syndrome

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21
Q

**Obesity directly assoc’d. with HTN:

A

– Increased body mass = Increased blood volume
– Adipocytes release angiotensinogen
– Adipocytes release profibrinogen & plasminogen
activator inhibitor = Increase Viscosity

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22
Q

Essential HTN and Metabolic syndrome (GHID)

A

Metabolic Syndrome:
• Increase atherogenic risk factors including HTN
• hypertiglyceridemia
• DECREASE HDL
• glucose intolerance and truncal obesity

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23
Q

Vascular resistance increases with age due to

A

medial hypertrophy as vessels adapt to prolonged pressure stress.

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24
Q

Essential HTN comprised ____% of patients
age of onset
Family hx of ____
Labs:

A 
90%
age of onset 20-50
Family hx of HTN
Increase Cr
Decrease K
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25
Q

What are the 2nd causes of HTN (CPP RCC)

A 
Chronic renal disease
Rrimary aldosteronism
Renovascular
Pheochromocytoma
Coarctation of Aorta
Cushing Syndrome
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26
Q

HTN carries increased risk of

A

post MI complication ex. ventricular wall rupture

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27
Q 
Secondary Hypertension 
Has\_\_\_\_\_
may required \_\_\_\_\_\_
Often \_\_\_\_
if untreated \_\_\_\_\_
A
  • Has defined structural or hormone cause.
  • May require different therapy from EH.
  • Often curable.
  • If untreated, adaptive changes lead to EH.
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28
Q

In general, causes for Secondary HTN can be: (MERE)

A

– Mechanical
–Exogenous
–Renal
– Endocrine

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29
Q

EXOGENOUS CAUSES

A 
Meds:
– Oral contraceptives increased renin secretion.
– Estrogen Increased hepatic angiotensinogen production.
– Glucocorticoids
– Cyclosporine
– Erythropoietin
– Sympathomimetic drugs
– (NSAIDs via  Na+ and water retention)
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30
Q

Renal parenchymal ds:Damaged nephrons

A

damaged nephrons cant excrete normal amounts of Na & water = Increase vol & C.O. = HTN

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31
Q

Renal parenchymal ds:Renal Artery stenosis

A

• Renal artery stenosis: one or both arteries lead to HTN
– Main Cause: Atherosclerosis
– Other Causes: emboli, vasculitis, external compression of renal artery

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32
Q

Renal parenchymal ds: Low perfusion pressure

A

= Increased Renin secretion

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33
Q

For unitlateral Artery disease

A

ACEI, contraindicated in bilateral renal stenosis

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34
Q

Avoid for Bilateral renal artery ds. –

A

inhib. of ANGIOGENSIN II production may excessively reduce intraglomerular pressure & filtration, and worsen renal function in pts with bilateral ds. who already have compromised perfusion to both kidneys.

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35
Q

Coartaction of Aorta (sometimes involves

A

L. subclav. = decrease Left arm pressures

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36
Q

What are the two mechanisms of COA

A

• 2 mechanisms:
– 1- reduced blood flow to kidneys stims. Renin.
– 2- high press prox to coarctation stiffens aortic arch thru
medial hyperplasia and accelerated atherosclerosis, blunting baroreceptor response to high pressures.

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37
Q

SIgns of COA (MICW)

A

– Mid-systolic murmur
- Inadequate flow to legs or left arm.
– Claudication or fatigue.
– Weak/Absent femoral pulses.

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38
Q

What are the ENDOCRINE CAUSES Of HTN

GMTP

A 
ENDOCRINE CAUSES
– Pheochromocytoma
– Mineralocorticoid
– Glucocorticoid
– Thyroid
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39
Q

Pheochromocytoma -

A

Adrenal medulla epi/norepi intermittent or chronic vasoconstriction, tachycardia & other SNS effects.

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40
Q

Signs and symptoms of Pheochromocytoma

PPTS

A

Severe throbbing HA
Profuse sweating
Palpitations
Tachycardia.

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41
Q

Diagnosis of Pheochromocytoma

A

Increases serum or urine catecholamine levels & their metabolites (vanillylmandelic acid and metanephrine)

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42
Q

Tx of Pheochromocytma

A

α-blocker phenoxybenzamine with β-blocker &
catecholamine biosynthesis inhibitor α-methyltyrosine,
Surgical resection

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43
Q

Secondary HTN endocrine causes of HTN Mineralocorticoid

A

ALdosterone

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44
Q

Primary aldosterone due to

A

From adrenal adenoma
Dx; obtain K level, urine, plasma renin and aldosterone
Tx: remove tumor

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45
Q

Secondary Aldosteronism -

A

from abnormally high ANGIOTENSIN II,

NO PROBLEM With Adrenal gland

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46
Q

3 causes of Secondary Aldosteronism RIO

A

– 1) rare renin-secreting tumor.
– 2) oral contaceptives - stim.s Liver to Increase angiotensinogen.
– 3) impaired ANGIOTENSIN II degradation in chronic liver ds.

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47
Q

Glucocorticoid-remediable Aldosteronism (GRA)

–

A

genetic rearrangement results in aldosterone synthesis

abnormally regulated by ACTH.

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48
Q

Hypertensive Crisis

A

Medical Emergency pressures >180/>110.

• Often caused by

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49
Q

Hypertensive crisis causes

A

acute hemodynamic insult superimposed on chronic HTN. (ex acute renal ds)

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50
Q

Glucocorticoids Dx

A

24 hours urine cortisol or DEXAMETHASONE

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51
Q

In Hypertensive crisis there is

A

• Severe pressure elevation = Increased ICP, hypertensive

encephalopathy (HA, blurred vision, confusion, somnolence, coma).

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52
Q

Hypertensive Crisis and eye

A

Retinal hemorrhages,exudates, papilledema seen

on fundoscopy

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53
Q

Hypertensive crisis tx

A 
Tx:
– nitroprusside (use with caution, can Increase ICP)
– labetalol
– fenoldopam
– nicardipine
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54
Q

Optic disk edema is ______means _____

A

PAPILLEDEMA; Increased ICP

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55
Q

Tx of HTN: Diuretics classes are

A

Thiazides
Potassium Sparing diuretics
LOOP diuretics

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56
Q

Physiological Action of diuretics

A

Decreased Circulating Volume

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57
Q

Sympatholytics classes are :

A

B blockers
Combined alpha and beta blockers
Central Alpha 2 agonists
Peripheral alpha 1 antagonists.

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58
Q

Physiologic actions of sympatholytics

A

Decrease HR, contractility and renin secretion
Vascular smooth muscle relaxation
Decrease sympathetic tone

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59
Q

Vasodilators classes are

A 
CCB 
Direct vasodilators (hydralazine)
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60
Q

PHysiologic actions of both CCB and direct vasodilators

A

Decrease PVR

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61
Q

Renin Angiotensin Aldosterone System angatonists ared

A

ACEIs
ARBs
Direct Renin Inhibitors

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62
Q

Physiologic actions of RAAS antagonists

A

Decrease PVR

Decrease sodium retention

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63
Q

Disease of Aorta subject to injury from________

A

mechanical trauma.

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64
Q

AORTA is continuously exposed to

A

high pulsatile pressure and shear stress.

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65
Q

IN AORTA• Elastin to collagen ration is _____And it _______

A

2:1 - allows expansion & recoil

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66
Q

In AORTA With age,

A

elastin degenerates, collagen becomes prominent = stiffening = Increases systolic press.

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67
Q

Diseases of the aorta appear as:

A
  • Aneurysm

* Dissection

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68
Q

Aneurysm is an

A

• abnormal localized dilation

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69
Q

In aneurysm diameter

A

• diameter increase of at least 50%

70
Q

What is a “True aneurysm” =

• manifest as _____and ____

A

dilatation of all three wall layers

fusiform or saccular

71
Q

False aneurysm AKA_______There is

A

Pseudoaneurysm

Hematoma contained by adventitia or PERIVASCULAR CLOT

72
Q

In false aneurysm there a

A

hole in media and intima

73
Q

Which one is more common fusiform or saccular? what is FUSIFORM

A

Fusiform

Symmetrical dilation of entire circumference of a segment

74
Q

Saccular is a

A

localized outpouching involving on a portion of the circumference

75
Q

Pseudoaneurysm “False aneurysm” =

A

Contained rupture of wall
blood leaks out of vessel through hole in intima and
media, but contained by adventitia or perivascular thrombus.

76
Q

Pseudoaneurysm warning

A

Very unstable, prone to complete rupture

77
Q

True aneurysm causes

A

Ascending thoracic aortic aneurysms

78
Q

TRUE ANEURYSM Also develops in certain genetic connective tissue disorders:
–MLE

A

Marfan syndrome
– Loeys-Dietz syndrome
– Ehlers Danlos syndrome (type IV)

79
Q

Descending thoracic & abdominal aortic

aneurysms

A

Assoc’d. with atherosclerosis.
Inflammation
INCREASED CRP and IL-6

80
Q

Thoracic aneurysms may compress
– Trachea or Mainstem bronchus =
= hoarseness

A

adjacent structures:

81
Q

TRACHEA or MAINSTEM BRONCHUS

A

cough, dyspnea, pneumonia

82
Q

If Thoracic aneurysms compress– Esophagus =

83
Q

If Thoracic aneurysms compress– Recurrent laryngeal nerve

A

HOARSENESS

84
Q

AORTIC DISSECTION is

A
  • Tear in intima allows blood into medial layer.

* Blood propagates along the plane of the muscle layer.

85
Q

AORTIC DISSECTION classifified as

A

CLASS A and CLASS B

86
Q

Type A is more

A

Devastating because potential extension into coronary arteries and arch vessels, support structures of aortic valve or pericardial
space.

87
Q

Clinical presentation of Type A

Pain travels_________can radiate anywhere in _____ or _____

A

Sudden severe pain with “tearing” or “ripping” in anterior chest (usually Type A) or between scapula (Type B).
– Pain travels along propagation, can radiate anywhere in
thorax or abdomen.
– (Painless dissection is possible but uncommon)

88
Q

Tearing or ripping in anterior chest is usually type

89
Q

Tearing or ripping in SCAPULA

90
Q

Complications of Aortic Dissection : RUPTURE

A

Pericardial tamponade
Hemomediastinum
Hemothorax (usually left side)

91
Q

Complications of Aortic Dissection : OCCLUSION or AROTIC BRANCH VESSELS (CCRIS)

A 
Carotid (stroke)
Coronary (MI) 
Renal (ARF)
Iliac, Brachiocephalic, Subclavian (limb ischemia) 
Splanchnic (visceral infection)
92
Q

Complications of Aortic Dissection: DISTORTION OF AORTIC ANNULUS

A

Aortic Regurgitation

93
Q

Diseases of Aorta: Immediate DX necessary with

A 
Contrast CT (CTA)
TEE
94
Q

Diseases of Aorta main goals for treatment

A

TX:
– Arrest progression of dissecting channel
– decrease systolic BP
– Decrease contractility to minimize wall shear

95
Q

Causes of PAD (VAT)

A

Causes:
– Vasculitis
– Atherosclerosis (most common)
– Thromboembolism

96
Q

Clinical presentation of PAD

A

Claudication, relieved by rest.

97
Q

Evaluation of PAD ABI

A

ABI (ankle-brachial index)

98
Q

– ABI > 1.0

99
Q

– ABI < 0.9

A

diagnostic of PAD

100
Q

– ABI < 0.5

101
Q

3 measures to evaluate PAD

A

ABI
Segmental pressures
PVR (pulse volume recordings)

102
Q

Treatment of PAD: ASA

A

antiplatelet therapy

103
Q

Treatment of PAD: Cilostazol

A

Phosphodiesterase inhibitor (increase cAMP for vasodilation; antiplatelet effect)

104
Q

Most dangerous aneurysm is

A

False aneurysms

105
Q

Treatment of PAD: Pentoxifylline

A

INCREASED RBC deformability, improves claudication

106
Q

PAD surgery

A

Surgical revascularization if medical therapy fails, or as first
line in severe limb ischemia

107
Q

Causes of Acute Arterial Occlusion

A

– Thrombus

– Embolism

108
Q

For acute arterial occlusion

A

Origin of arterial emboli most often the heart.

Rarely from venous, unless passing through abnormal intracardiac shunt (ex. ASD) = “paradoxical embolism”

109
Q

Signs of PAD , 5 Ps

Tx

A 
Signs/symptoms: "five Ps"
– Pain
– Pallor
– Paralysis
– Paresthesia
– Pulselessness
– Poikilothermia (coolness)

Anticoagulants: heparin

110
Q

PAD : VASCULITIS SYNDROMES are (GTT)

A

– Takayasu arteritis
– Giant cell arteritis (Temporal arteritis)
– Thromboangitis obliterans (Buerger disease)

111
Q

Takayasu Arteritis most commonly affected is

A

Aorta and its branches

112
Q

Giant Cell ARTERITIS most commonly affected ______-as well as_________

A

Medium to Large vessels (especially cranial vessels) as well as aortic arch and branches

113
Q

Thromboangiitis obliterans ( Buerger disease) most commonly affected

A

small size (especially distal arteries and extremities)

114
Q

PAD : VASOSPASM:

A

RAYNAUD PHENOMENON

115
Q

What is raynaud phenomenon?

A

• Extreme vasospasm of digits in response to cold

temperatures

116
Q

Raynaud phenomenon when there is Temporarily inhibits blood flow =

A

painful transient ischemia

117
Q

• Triphasic color response in digits in RAYNAUD’s

A

blanch (white) Phase I
– cyanosis (blue) - PHase II
– erythema (red- PHASE III

118
Q

Most aneurysm occurs in

A

Ascending Aorta TYPE A

119
Q

Venous diseases appear as:

A
  • Varicose Veins (1o & 2o)

* Venous Thrombus (DVT & PE)

120
Q

Varicose veins are

A

dilated, tortuous superficial vessels

121
Q

Primary Varicose veins originate in the

A

superficial system

122
Q

Causes of Varicose veins

A

– pregnancy
– prolonged standing
– obesity

123
Q

SECONDARY varicose veins

A

Varicose veins occur when an abnormality in the Deep system causes superficial varicosities.

124
Q

• Venous Thrombus “Thrombophlebitis”

A

• Superfical or Deep thrombus

125
Q

Most common site of DVT

A

– femoral
– iliac
– calves
– popliteal

126
Q

PE

• Often fatal.

A

• when clot embolism travels to lung.

127
Q

PE: occurrence

A

600,000 per year in U.S.

128
Q

PE and gas exchanged•

A

Gas exchange is impaired = V/Q mismatch.

129
Q

PE patho

A

• Increase pulmonary vasc. resistance = elevation RV wall stress,
dilation and failure.

130
Q

Virchow’s Triad are

A

Factors that predispose to Venous thrombosis

131
Q

The triad of Virchow’s is (VHS)

A

a. Stasis of blood flow
b. Hypercoagulable state
c. Vascular diseas

132
Q

Virchow’s Triad STASIS of BLOOD FLOW (PIHH)

A

Prolonged inactivity
Immobilized extremity
Heart failure
Hyperviscosity syndrome

133
Q

Prolonged inactivity examples

A

surgery, prolonged travel

134
Q

Immobilized extremity examples

A

Following bone fracture

135
Q

Heart failure in stasis of blood flow

A

Systemic venous congestions

136
Q

Examples of hyperviscosity syndromE

A

Polycythemia Vera

137
Q

Hypercoagulable state Disease (FPANPMS)

A 
Factor V leiden deficienty
Prothrombin gene mutation
Antithrombin, Protein C and S deficiency
Neoplastic disease(lung breast CA) 
Pregnancy 
Myeloproliferative disease
Smoking
138
Q

Vascular damage examples

A

Instrumentation ( IV catheters)

Trauma

139
Q

Clinical Presentation of DVT (ALULETH)

A 
Asymptomatic in some pts.
• Leg pain
• Unilateral leg swelling
• localized warmth
• Erythema
• Tenderness over phlebitic
vein
• +Homans' sign (nonspecific)
140
Q

Clinical presentation of PE: (DPHSCTB)

A 
dyspnea
• pleuritic chest pain
• hemoptysis
• cough
• syncope
• tachypnea
• bronchospasm
141
Q

SUPERFICIAL THROMBOPHLEBITIS
What is it?
Sometimes a complication of _______
Does it lead to PE?

A

inflammation & thrombus superficial vein.
• sometimes a complication of in-dwelling intravenous catheter.
• does not lead to PE.

142
Q

Tx of venous disease intervention

A

Wear compression stockings

Elevate Legs

143
Q

Tx of PAD interventions (CAW)

A

Control smoking
Wear insulated gloves
Avoid cold environments

144
Q

Ischemic ulcers characteristics (PWD)

A
  • “punched out” appearance
  • well defined edges
  • Deeper wound base
145
Q

Venous insufficiency Characteristics (SLMR)

A

Less defined edge
Shallow wound base
More proximal, medial on leg
Reddish-brown hemosiderin deposits.

146
Q

Not so obvious signs of PAD

A

Loss of pulses distal to stenosis

– Bruits may be audible over sites of stenosis

147
Q

Treatment of AORTA diseases
– based on___________
– Surgical repair while pt. maintained_________
– Aneurysm resected and replaced with prosthetic Dacron
graft.

A

size & pts. overall condition

on cardiopulmonary bypass.

148
Q

Medical therapy of AORTA DISEASES

A

– β-blockers (reduce expansion rate)

– smoking cessation

149
Q 
Other symptoms of AORTA disease
Clinical Presentation:
• Most aneurysms \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
some patients feel \_\_\_\_\_\_\_\_\_
• Can cause \_\_\_\_\_\_\_ \_\_\_\_\_\_
A

• Most aneurysms asymptomatic.
• Some pts. with AAA feel pulsatile mass.
• Can cause abdominal/back pain or vague GI
symptoms.

150
Q

Infection that can cause disease of Aorta (SSS TSF)

A 
Infections:
– Salmonella
– Staph
– Strep
– TB
– Syphilis
– Fungi
151
Q

**Ascending thoracic aortic aneurysms
Characterized by cystic
• Assoc’d. with _____ and ____

A

medial degeneration (“cystic medial necrosis”) = degeneration/fragmentation of elastic fibers in
medial layer.
aging and HTN.

152
Q

Ascending thoracic aortic aneurysm may_____Causing______ and _________

A

May dilate aortic ring = aortic regurg. & symptoms of CHF

153
Q

Caused by 3 categories of processes–> PAD

A 
1.Structural wall changes secondary to degenerative conditions,
infection, inflammation – lead to:
• Dilation
• Aneurysm
• Dissection / Rupture
  1. Stenosis of lumen secondary to atherosclerosis, thrombus or inflammation.
  2. Spasm of vascular smooth muscle.
154
Q

Non-pharmacologic of Treatment of HTN

A

• Wgt. reduction, exercise, diet, sodium restriction,

cessation alcohol & tobacco (relaxation therapy)

155
Q

Renal causes: Secondary HTN
Renal artery stenosis is
Main cause _______
Other causes : –> EVE

A

• Renal artery stenosis: one or both arteries lead to HTN
– Main Cause: Atherosclerosis
– Other Causes: emboli, vasculitis, external compression of renal artery

156
Q

***2nd HTN: Hx recurrent UTI - could =

A

chronic pyelonephritis = renal damage = HTN

157
Q

***2nd HTN: excessive wgt loss

A

could = pheochromocytoma = excess SNS stim = HTN

158
Q

***2nd HTN:– excessive wgt gain

A

could = cushing syndrome = excess glucocorts/aldost. = HTN

159
Q 
***Secondary HTN (compared to HTN) 
Age : \_\_\_\_\_\_\_
Severity: 
Onset
Associated S/S
A

Age - if HTN develops age <20 or >50
• Severity - pressure rises dramatically vs. Essential Hypertension mild to moderate
• Onset - presents abruptly in previous normotensive
vs. gradual over yrs in EH
• Assoc’d signs/symptoms - renal artery bruit heard
on abd. exam in pt w/ renal a. stenosis

160
Q

HTN: organ damage

HAAFE

A 
Heart wall stress
Aorta damage (increase risk aneurysm)
Arterial damage, accelerated atherosclerosis via smooth muscle hypertrophy,
Fatigued elastic fibers
Endothelial cell dysfunction and
161
Q

HTN organ damage : thrombosis

A

Increase risk of thrombosis and embolism damage target

organs

162
Q

How does Pressure natriuresis work ?

A

increasing renal sodium excretion when incoming arterial pressure to the kidneys rises.

163
Q

Signals sent to Medulla Oblongata: when BP high

A

– Increase BP causes rate of signals to rise, inhibits vasomotor center, DECREASES sympathetic tone, vasodilation causes BP to decrease

164
Q

Signals sent to Medulla Oblongata: when BP LOW

A

BP causes rate of signals to drop, excites vasomotor center, INCREASE sympathetic tone, vasoconstriction and BP INCREASES

165
Q

Hematocrit on BP

166
Q

NP on BP

167
Q

Aldosterone on BP

168
Q

{H+} concentration on BP

169
Q

Which organ has the most potential control over BP

170
Q

Insulin resistance/ DM

A

HTN patients with obesity or type II diabetes have increase glucose –> Increase insulin results in increase sympathetic activation, contributes to HTN

171
Q

Increase insulin also stimulates what?

A

Vasoconstriction smooth muscle hypertrophy = Increase vascular resistance

172
Q

Smooth muscle hypertrophy also caused by

A

direct mitogenic effect of insulin or Increase sensitivity to PDGF

SRNAAnatomy II (16 decks)

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