Hypertension Flashcards
(172 cards)
1
Q
– Primary HTN (essential)
A
cause is unknown (~90% of cases)
2
Q
– Secondary HTN
A
has definable cause (less common)
3
Q
Normal Blood pressure
A
SBP Less than 120
DBP less than 80
4
Q
Pre HTN
A
SBP 120-139
DBP 80-89
5
Q
Stage I HTN
A
SBP 140-159
DBP 90-99
6
Q
Stage II HTN
A
SBP >160
DBP > 90
7
Q
Hypertensive Crisis
A
SBP >180
DBP>110
8
Q
B2 receptors on PVR
A
Decreases
9
Q
Local regulators: Nitrous oxide on PVR
A
Decreases
10
Q
Local regulators: Adenosine on PVR
A
Decreases
11
Q
Local regulators: Prostaglandins on PVR
A
Decreases
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
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
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)
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.
16
Q
HTN Abnormalities
A
Heart, Blood Vessels & Kidney
Also contribute to development HTN.
17
Q
HTN and heart
A
HEART
– Increased C.O. – HTN pts. have excessive sympathetic response under psychologically stressful conditions.
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
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.
20
Q
ESSENTIAL HTN : Other genetic factors (IOM)
A
Other genetically linked factors:
– Insulin resistance/DM
– Obesity
– Metabolic Syndrome
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
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
23
Q
Vascular resistance increases with age due to
A
medial hypertrophy as vessels adapt to prolonged pressure stress.
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
25
What are the 2nd causes of HTN (CPP RCC)
```
Chronic renal disease
Rrimary aldosteronism
Renovascular
Pheochromocytoma
Coarctation of Aorta
Cushing Syndrome
```
26
HTN carries increased risk of
post MI complication ex. ventricular wall rupture
27
```
Secondary Hypertension
Has_____
may required ______
Often ____
if untreated _____
```
- Has defined structural or hormone cause.
- May require different therapy from EH.
- Often curable.
- If untreated, adaptive changes lead to EH.
28
In general, causes for Secondary HTN can be: (MERE)
– Mechanical
–Exogenous
–Renal
– Endocrine
29
EXOGENOUS CAUSES
```
Meds:
– Oral contraceptives increased renin secretion.
– Estrogen Increased hepatic angiotensinogen production.
– Glucocorticoids
– Cyclosporine
– Erythropoietin
– Sympathomimetic drugs
– (NSAIDs via Na+ and water retention)
```
30
Renal parenchymal ds:Damaged nephrons
damaged nephrons cant excrete normal amounts of Na & water = Increase vol & C.O. = HTN
31
Renal parenchymal ds:Renal Artery stenosis
• Renal artery stenosis: one or both arteries lead to HTN
– Main Cause: Atherosclerosis
– Other Causes: emboli, vasculitis, external compression of renal artery
32
Renal parenchymal ds: Low perfusion pressure
= Increased Renin secretion
33
For unitlateral Artery disease
ACEI, contraindicated in bilateral renal stenosis
34
Avoid for Bilateral renal artery ds. –
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.
35
Coartaction of Aorta (sometimes involves
L. subclav. = decrease Left arm pressures
36
What are the two mechanisms of COA
• 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.
37
SIgns of COA (MICW)
– Mid-systolic murmur
- Inadequate flow to legs or left arm.
– Claudication or fatigue.
– Weak/Absent femoral pulses.
38
What are the ENDOCRINE CAUSES Of HTN
| GMTP
```
ENDOCRINE CAUSES
– Pheochromocytoma
– Mineralocorticoid
– Glucocorticoid
– Thyroid
```
39
Pheochromocytoma -
Adrenal medulla epi/norepi intermittent or chronic vasoconstriction, tachycardia & other SNS effects.
40
Signs and symptoms of Pheochromocytoma
| PPTS
Severe throbbing HA
Profuse sweating
Palpitations
Tachycardia.
41
Diagnosis of Pheochromocytoma
Increases serum or urine catecholamine levels & their metabolites (vanillylmandelic acid and metanephrine)
42
Tx of Pheochromocytma
α-blocker phenoxybenzamine with β-blocker &
catecholamine biosynthesis inhibitor α-methyltyrosine,
Surgical resection
43
Secondary HTN endocrine causes of HTN Mineralocorticoid
ALdosterone
44
Primary aldosterone due to
From adrenal adenoma
Dx; obtain K level, urine, plasma renin and aldosterone
Tx: remove tumor
45
Secondary Aldosteronism -
from abnormally high ANGIOTENSIN II,
| NO PROBLEM With Adrenal gland
46
3 causes of Secondary Aldosteronism RIO
– 1) rare renin-secreting tumor.
– 2) oral contaceptives - stim.s Liver to Increase angiotensinogen.
– 3) impaired ANGIOTENSIN II degradation in chronic liver ds.
47
Glucocorticoid-remediable Aldosteronism (GRA)
| –
genetic rearrangement results in aldosterone synthesis
| abnormally regulated by ACTH.
48
Hypertensive Crisis
Medical Emergency pressures >180/>110.
| • Often caused by
49
Hypertensive crisis causes
acute hemodynamic insult superimposed on chronic HTN. (ex acute renal ds)
50
Glucocorticoids Dx
24 hours urine cortisol or DEXAMETHASONE
51
In Hypertensive crisis there is
• Severe pressure elevation = Increased ICP, hypertensive
| encephalopathy (HA, blurred vision, confusion, somnolence, coma).
52
Hypertensive Crisis and eye
Retinal hemorrhages,exudates, papilledema seen
| on fundoscopy
53
Hypertensive crisis tx
```
Tx:
– nitroprusside (use with caution, can Increase ICP)
– labetalol
– fenoldopam
– nicardipine
```
54
Optic disk edema is ______means _____
PAPILLEDEMA; Increased ICP
55
Tx of HTN: Diuretics classes are
Thiazides
Potassium Sparing diuretics
LOOP diuretics
56
Physiological Action of diuretics
Decreased Circulating Volume
57
Sympatholytics classes are :
B blockers
Combined alpha and beta blockers
Central Alpha 2 agonists
Peripheral alpha 1 antagonists.
58
Physiologic actions of sympatholytics
Decrease HR, contractility and renin secretion
Vascular smooth muscle relaxation
Decrease sympathetic tone
59
Vasodilators classes are
```
CCB
Direct vasodilators (hydralazine)
```
60
PHysiologic actions of both CCB and direct vasodilators
Decrease PVR
61
Renin Angiotensin Aldosterone System angatonists ared
ACEIs
ARBs
Direct Renin Inhibitors
62
Physiologic actions of RAAS antagonists
Decrease PVR
| Decrease sodium retention
63
Disease of Aorta subject to injury from________
mechanical trauma.
64
AORTA is continuously exposed to
high pulsatile pressure and shear stress.
65
IN AORTA• Elastin to collagen ration is _____And it _______
2:1 - allows expansion & recoil
66
In AORTA With age,
elastin degenerates, collagen becomes prominent = stiffening = Increases systolic press.
67
Diseases of the aorta appear as:
* Aneurysm
| * Dissection
68
Aneurysm is an
• abnormal localized dilation
69
In aneurysm diameter
• diameter increase of at least 50%
70
What is a "True aneurysm" =
| • manifest as _____and ____
dilatation of all three wall layers
| fusiform or saccular
71
False aneurysm AKA_______There is
Pseudoaneurysm
| Hematoma contained by adventitia or PERIVASCULAR CLOT
72
In false aneurysm there a
hole in media and intima
73
Which one is more common fusiform or saccular? what is FUSIFORM
Fusiform
| Symmetrical dilation of entire circumference of a segment
74
Saccular is a
localized outpouching involving on a portion of the circumference
75
Pseudoaneurysm "False aneurysm" =
Contained rupture of wall
blood leaks out of vessel through hole in intima and
media, but contained by adventitia or perivascular thrombus.
76
Pseudoaneurysm warning
Very unstable, prone to complete rupture
77
True aneurysm causes
Ascending thoracic aortic aneurysms
78
TRUE ANEURYSM Also develops in certain genetic connective tissue disorders:
–MLE
Marfan syndrome
– Loeys-Dietz syndrome
– Ehlers Danlos syndrome (type IV)
79
Descending thoracic & abdominal aortic
| aneurysms
Assoc'd. with atherosclerosis.
Inflammation
INCREASED CRP and IL-6
80
Thoracic aneurysms may compress
– Trachea or Mainstem bronchus =
= hoarseness
adjacent structures:
81
TRACHEA or MAINSTEM BRONCHUS
cough, dyspnea, pneumonia
82
If Thoracic aneurysms compress– Esophagus =
dysphagia
83
If Thoracic aneurysms compress– Recurrent laryngeal nerve
HOARSENESS
84
AORTIC DISSECTION is
* Tear in intima allows blood into medial layer.
| * Blood propagates along the plane of the muscle layer.
85
AORTIC DISSECTION classifified as
CLASS A and CLASS B
86
Type A is more
Devastating because potential extension into coronary arteries and arch vessels, support structures of aortic valve or pericardial
space.
87
Clinical presentation of Type A
Pain travels_________can radiate anywhere in _____ or _____
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
Tearing or ripping in anterior chest is usually type
A
89
Tearing or ripping in SCAPULA
B
90
Complications of Aortic Dissection : RUPTURE
Pericardial tamponade
Hemomediastinum
Hemothorax (usually left side)
91
Complications of Aortic Dissection : OCCLUSION or AROTIC BRANCH VESSELS (CCRIS)
```
Carotid (stroke)
Coronary (MI)
Renal (ARF)
Iliac, Brachiocephalic, Subclavian (limb ischemia)
Splanchnic (visceral infection)
```
92
Complications of Aortic Dissection: DISTORTION OF AORTIC ANNULUS
Aortic Regurgitation
93
Diseases of Aorta: Immediate DX necessary with
```
Contrast CT (CTA)
TEE
```
94
Diseases of Aorta main goals for treatment
TX:
– Arrest progression of dissecting channel
– decrease systolic BP
– Decrease contractility to minimize wall shear
95
Causes of PAD (VAT)
Causes:
– Vasculitis
– Atherosclerosis (most common)
– Thromboembolism
96
Clinical presentation of PAD
Claudication, relieved by rest.
97
Evaluation of PAD ABI
ABI (ankle-brachial index)
98
– ABI > 1.0
normal
99
– ABI < 0.9
diagnostic of PAD
100
– ABI < 0.5
severe
101
3 measures to evaluate PAD
ABI
Segmental pressures
PVR (pulse volume recordings)
102
Treatment of PAD: ASA
antiplatelet therapy
103
Treatment of PAD: Cilostazol
Phosphodiesterase inhibitor (increase cAMP for vasodilation; antiplatelet effect)
104
Most dangerous aneurysm is
False aneurysms
105
Treatment of PAD: Pentoxifylline
INCREASED RBC deformability, improves claudication
106
PAD surgery
Surgical revascularization if medical therapy fails, or as first
line in severe limb ischemia
107
Causes of Acute Arterial Occlusion
– Thrombus
| – Embolism
108
For acute arterial occlusion
Origin of arterial emboli most often the heart.
| Rarely from venous, unless passing through abnormal intracardiac shunt (ex. ASD) = “paradoxical embolism”
109
Signs of PAD , 5 Ps
| Tx
```
Signs/symptoms: "five Ps"
– Pain
– Pallor
– Paralysis
– Paresthesia
– Pulselessness
– Poikilothermia (coolness)
```
Anticoagulants: heparin
110
PAD : VASCULITIS SYNDROMES are (GTT)
– Takayasu arteritis
– Giant cell arteritis (Temporal arteritis)
– Thromboangitis obliterans (Buerger disease)
111
Takayasu Arteritis most commonly affected is
Aorta and its branches
112
Giant Cell ARTERITIS most commonly affected ______-as well as_________
Medium to Large vessels (especially cranial vessels) as well as aortic arch and branches
113
Thromboangiitis obliterans ( Buerger disease) most commonly affected
small size (especially distal arteries and extremities)
114
PAD : VASOSPASM:
RAYNAUD PHENOMENON
115
What is raynaud phenomenon?
• Extreme vasospasm of digits in response to cold
| temperatures
116
Raynaud phenomenon when there is Temporarily inhibits blood flow =
painful transient ischemia
117
• Triphasic color response in digits in RAYNAUD's
blanch (white) Phase I
– cyanosis (blue) - PHase II
– erythema (red- PHASE III
118
Most aneurysm occurs in
Ascending Aorta TYPE A
119
Venous diseases appear as:
* Varicose Veins (1o & 2o)
| * Venous Thrombus (DVT & PE)
120
Varicose veins are
dilated, tortuous superficial vessels
121
Primary Varicose veins originate in the
superficial system
122
Causes of Varicose veins
– pregnancy
– prolonged standing
– obesity
123
SECONDARY varicose veins
Varicose veins occur when an abnormality in the **Deep system** causes superficial varicosities.
124
• Venous Thrombus "Thrombophlebitis"
• Superfical or Deep thrombus
125
Most common site of DVT
– femoral
– iliac
– calves
– popliteal
126
PE
| • Often fatal.
• when clot embolism travels to lung.
127
PE: occurrence
600,000 per year in U.S.
128
PE and gas exchanged•
Gas exchange is impaired = V/Q mismatch.
129
PE patho
• Increase pulmonary vasc. resistance = elevation RV wall stress,
dilation and failure.
130
Virchow’s Triad are
Factors that predispose to Venous thrombosis
131
The triad of Virchow's is (VHS)
a. Stasis of blood flow
b. Hypercoagulable state
c. Vascular diseas
132
Virchow's Triad STASIS of BLOOD FLOW (PIHH)
Prolonged inactivity
Immobilized extremity
Heart failure
Hyperviscosity syndrome
133
Prolonged inactivity examples
surgery, prolonged travel
134
Immobilized extremity examples
Following bone fracture
135
Heart failure in stasis of blood flow
Systemic venous congestions
136
Examples of hyperviscosity syndromE
Polycythemia Vera
137
Hypercoagulable state Disease (FPANPMS)
```
Factor V leiden deficienty
Prothrombin gene mutation
Antithrombin, Protein C and S deficiency
Neoplastic disease(lung breast CA)
Pregnancy
Myeloproliferative disease
Smoking
```
138
Vascular damage examples
Instrumentation ( IV catheters)
| Trauma
139
Clinical Presentation of DVT (ALULETH)
```
Asymptomatic in some pts.
• Leg pain
• Unilateral leg swelling
• localized warmth
• Erythema
• Tenderness over phlebitic
vein
• +Homans' sign (nonspecific)
```
140
Clinical presentation of PE: (DPHSCTB)
```
dyspnea
• pleuritic chest pain
• hemoptysis
• cough
• syncope
• tachypnea
• bronchospasm
```
141
SUPERFICIAL THROMBOPHLEBITIS
What is it?
Sometimes a complication of _______
Does it lead to PE?
inflammation & thrombus superficial vein.
• sometimes a complication of in-dwelling intravenous catheter.
• does not lead to PE.
142
Tx of venous disease intervention
Wear compression stockings
| Elevate Legs
143
Tx of PAD interventions (CAW)
Control smoking
Wear insulated gloves
Avoid cold environments
144
Ischemic ulcers characteristics (PWD)
- "punched out" appearance
- well defined edges
- Deeper wound base
145
Venous insufficiency Characteristics (SLMR)
Less defined edge
Shallow wound base
More proximal, medial on leg
Reddish-brown hemosiderin deposits.
146
Not so obvious signs of PAD
Loss of pulses distal to stenosis
| – Bruits may be audible over sites of stenosis
147
Treatment of AORTA diseases
– based on___________
– Surgical repair while pt. maintained_________
– Aneurysm resected and replaced with prosthetic Dacron
graft.
size & pts. overall condition
| on cardiopulmonary bypass.
148
Medical therapy of AORTA DISEASES
– β-blockers (reduce expansion rate)
| – smoking cessation
149
```
Other symptoms of AORTA disease
Clinical Presentation:
• Most aneurysms __________________
some patients feel _________
• Can cause _______ ______
```
• Most aneurysms asymptomatic.
• Some pts. with AAA feel pulsatile mass.
• Can cause abdominal/back pain or vague GI
symptoms.
150
Infection that can cause disease of Aorta (SSS TSF)
```
Infections:
– Salmonella
– Staph
– Strep
– TB
– Syphilis
– Fungi
```
151
****Ascending thoracic aortic aneurysms
Characterized by cystic
• Assoc'd. with _____ and ____
medial degeneration ("cystic medial necrosis") = degeneration/fragmentation of elastic fibers in
medial layer.
aging and HTN.
152
Ascending thoracic aortic aneurysm may_____Causing______ and _________
May dilate aortic ring = aortic regurg. & symptoms of CHF
153
Caused by 3 categories of processes--> PAD
```
1.Structural wall changes secondary to degenerative conditions,
infection, inflammation – lead to:
• Dilation
• Aneurysm
• Dissection / Rupture
```
2. Stenosis of lumen secondary to atherosclerosis, thrombus or inflammation.
3. Spasm of vascular smooth muscle.
154
Non-pharmacologic of Treatment of HTN
• Wgt. reduction, exercise, diet, sodium restriction,
| cessation alcohol & tobacco (relaxation therapy)
155
Renal causes: Secondary HTN
Renal artery stenosis is
Main cause _______
Other causes : --> EVE
• Renal artery stenosis: one or both arteries lead to HTN
– Main Cause: Atherosclerosis
– Other Causes: emboli, vasculitis, external compression of renal artery
156
***2nd HTN: Hx recurrent UTI - could =
chronic pyelonephritis = renal damage = HTN
157
***2nd HTN: excessive wgt loss
could = pheochromocytoma = excess SNS stim = HTN
158
***2nd HTN:– excessive wgt gain
could = cushing syndrome = excess glucocorts/aldost. = HTN
159
```
***Secondary HTN (compared to HTN)
Age : _______
Severity:
Onset
Associated S/S
```
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
HTN: organ damage
| HAAFE
```
Heart wall stress
Aorta damage (increase risk aneurysm)
Arterial damage, accelerated atherosclerosis via smooth muscle hypertrophy,
Fatigued elastic fibers
Endothelial cell dysfunction and
```
161
HTN organ damage : thrombosis
Increase risk of thrombosis and embolism damage target
| organs
162
How does Pressure natriuresis work ?
increasing renal sodium excretion when incoming arterial pressure to the kidneys rises.
163
Signals sent to Medulla Oblongata: when BP high
– Increase BP causes rate of signals to rise, inhibits vasomotor center, DECREASES sympathetic tone, vasodilation causes BP to decrease
164
Signals sent to Medulla Oblongata: when BP LOW
BP causes rate of signals to drop, excites vasomotor center, INCREASE sympathetic tone, vasoconstriction and BP INCREASES
165
Hematocrit on BP
Increase
166
NP on BP
decreases
167
Aldosterone on BP
Increase
168
{H+} concentration on BP
Decrease
169
Which organ has the most potential control over BP
Kidneys
170
Insulin resistance/ DM
HTN patients with obesity or type II diabetes have increase glucose --> Increase insulin results in increase sympathetic activation, contributes to HTN
171
Increase insulin also stimulates what?
Vasoconstriction smooth muscle hypertrophy = Increase vascular resistance
172
Smooth muscle hypertrophy also caused by
direct mitogenic effect of insulin or Increase sensitivity to PDGF
