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SRNAAnatomy II > EXAM 4 REVIEW-Old > Flashcards

EXAM 4 REVIEW-Old Flashcards

1
Q

Concentration Gradients Example.

A

Extracellular Na+ ~142 mEq; intracellular Na+ ~14 mEq

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2
Q

For concentration gradient strong forces

A

Strong force tends to drive Na+ into cell, down it’s concentration gradient

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3
Q

Transmembrane potential: at rest

A

At rest inside cell is ~ -90 mV

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4
Q

T/F Strong electrical attraction for Na+ to enter cell

A

True

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5
Q

Cardiac myocytes have what kind of NA channels

A

“Fast Na+ Channels”

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6
Q

For cardiac myocytes, when the Na channels are open, important to know that

A

When activated remain open for only a few thousandths of a second, then close

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7
Q

Inactivated state persists until

A

membrane is repolarized, providing refractory period

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8
Q

Na channels not active on

A

Not active on pacemaker cells (SA/AV nodes

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9
Q

• K+ concentration normally greater______ cell due to_________ How many Na in and how many K out?

A

inside; sodium-potassium pump (3 Na out; 2 K in)

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10
Q

K Inward rectifier channels -

A

open in resting state allow some K+ to flow out of cell, but overall negative interior charge slows K+ outflow

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11
Q

What happens at equillibrium

A

At equilibrium, these forces are balanced and there

is zero net movement of K+

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12
Q

• K+ equilibrium potential is ___calculated by____

A

-91mV; Calculated by Nernst Equation: RT/ZF

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13
Q

For K+, because there is a slight leak of Na+ ions

into cell at rest,

A

actual resting potential is -90mV

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14
Q

Resting state before depolarization is known as

A

Phase 4

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15
Q

Phase 4

A

Rectifier channels leak K+ out

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16
Q

Phase 0

A

: Fast Na+ channels = rapid Na+ influx

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17
Q

Phase 1

A

Transient K+ channels open = K+ efflux

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18
Q

Phase 2:

A

L-type Ca++ channels type Ca++ channels = Ca++ influx
Delayed-rectifier channels = K+ efflux(plateau)
Ryanodine receptors: release Ca++ from S.R.

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19
Q

Phase 3:

A

Ca++ channels close Delayed-rectifier channels stay open until membrane potential reaches -90mV

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20
Q

“Fibrous Skeleton” of the heart is the

A

Fibrous connective tissue that surrounds the AV valves

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21
Q

The fibrous skeleton serve as

A

– Serves as electrical insulator, isolates Atria and Ventricles

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22
Q

What is the only conductor to the ventricles?

A

– AV node is the only electrical conductor to the Ventricles

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23
Q

What is the purpose of the delay at AV node?

A

Delay at AV node (0.1sec) allows atria time to contract before ventricles

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24
Q

What serves as an ELECTRICAL GATEKEEPER?

A

AV Node serves as electrical “gatekeeper” to limit

ventricular stim. during abnormal rapid atrial rhythms

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25
Q

SA node firing rate

A

60-100

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26
Q

AV node firing rate

A

40-60

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27
Q

Purkinje Fibers

A

30-40

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28
Q

Cells of conducting system have different

A

rates of firing

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29
Q

Normally _____node dominates.

A

SA

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30
Q

Under abnormal conditions, other pacemakers can

A

accelerate and overdrive the SA node

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31
Q

What is “Overdrive Suppression?

A

• Fastest cells preempt all others

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32
Q

Hexaxial (Limb) Leads in what plane?

A

(look in frontal plane)

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33
Q

Einthoven’s triangle – Leads

A

I, II, III

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34
Q

Bipolar (+) and (-) poles

A

I, II, III

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35
Q

Unipolar leads

A

aVR, aVL, aVF

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36
Q

Precordial Leads looks into what plane?

A

look in transverse plane)

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37
Q

Precardial leads are

A

V1 through V6

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38
Q

Lead views I, aVL:

A

lateral

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39
Q

Lead view II, III, aVF:

A

inferior

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40
Q

Lead view aVR:

A

superiomedial

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41
Q

P wave abnormalities: Atrial Enlargement

• Best seen in leads ______

A

Lead II & V1

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42
Q

RA depol. almost immediately followed by

A

LA depol. Both superimposed.

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43
Q

Lead II view is _____, which plane?

A

┴ to axis; Frontal plane

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44
Q

P wave abnormalities Atrial Enlargement

• Lead V1 view which plane?

A

• Transverse plane

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45
Q

First sign of MI

A

• STEMI (ST segment elevation myocardial infarction)

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46
Q

Ventricular repolarization very sensitive to

A

perfusion.

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47
Q

Pathological Q waves develop where ?

A

Develop in leads overlying infarcted tissue

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48
Q

Permanent evidence of MI

A

Pathological Q waves

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49
Q

Pathological Q waves occur where?

A

Occur in groups of leads

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50
Q

Pathologic Q waves do not do this?

A

Don’t indicate when injury occurred – could be

acute or years ago

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51
Q

Explain pathological Q waves

A

• Dead infarcted tissue under lead has no electrical
activity, acts as a ‘window’ for lead to see opposite
side of heart depolarizing away from lead
• Causes downward deflecting pathological Q wave

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52
Q

SVT rate

A

140-250 bpm

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53
Q

Where is SVT initiated?

A

Initiated by tissue at or above AV node

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54
Q

SVT Symptoms are

A

lightheaded, dizzy, fatigue, dyspnea

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55
Q

SVT and urine

A

Polyuria can be assoc’d. w/ SVT 2 to ANP (response to
↑atrial pressure from atrial contraction against closed AV
valve)

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56
Q

Which arrhythmia is associated with polyuria?

A

SVT

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57
Q

EKG in SVT have

A

P wave hidden in QRS

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58
Q

SVT management anesthesia

A

Avoid precipitating factors: ↑sympathetic tone,

electrolyte imbalances, acid-base disturbances

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59
Q

SVT tx If pt. hemodynamically stable, treat with

A

Vagal maneuvers and verbal reassurance

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60
Q

SVT If vagal ineffective, pharmacologic treatment should

be directed toward (ABC)

A

Blocking AV node conduction:

Adenosine, Beta-blockers. Calcium channel blockers

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61
Q

What medication is NOT useful with treatment of SVT?

A

Digoxin not useful 2o to delayed effect

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62
Q

SVT treatment if unresponsive to drugs

A

Electrical Cardioversion

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63
Q

Most important clinical consequence of AF is

A

Thromboembolic event causing stroke

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64
Q

Pharmacological conversion of atrial fibrillation

A

Normally, Pharm. Cardioversion with Class IC or III

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65
Q

Diseases that cause atrial enlargement promote

A

AFib

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66
Q

Afib causing diseases

A

HF, HTN, CAD, pulmonary ds., thyrotoxicosis, EtOH

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67
Q

No P wave; chaotic atria; irregular QRS

A

Afib

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68
Q

Afib If prior to induction

A

postpone surgery.

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69
Q

If AFIB occurs during anesthesia/surgery, and if hemodynamically significant,

A

Cardioversion chemically or electrically (syncd. @ 100-200J).

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70
Q

AFIB Ventricular rate control with drugs if vital signs

stable 3 drugs, drugs choice depends on what?

A

IV amiodarone, diltiazem or verapamil (drug choice depends on co-existing disease).

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71
Q

AF present for >48 hrs. predisposes to ______what do you have to do before cardioversion?

A

thrombus. Anticoag. for min. 3 wks. prior to electr.

Cardioversion.

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72
Q

Other alternative to anticoagulation for Afib

A

TEE to evaluate for thrombus, if none found, then electriccardiovert is lower risk)

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73
Q

MAT most commonly seen in

A

Most commonly seen in pt.s experiencing acute exacerbation of chronic lung disease.

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74
Q

Rhythm that Can also be assoc’d. w/ methylxanthine toxicity, CHF, sepsis, electrolyte abnormalities

A

MAT

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75
Q

How do you treat Multifocal Atria Tachycardia (MAT)

A

Usually responds to treatment of underlying pulmonary

decompensation with bronchodilators and supplemental O2.

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76
Q

Variable P wave morphology; irregular rhythm, what rhythm

A

MAT

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77
Q

PACs arise from

A

Ectopic foci in atria

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78
Q

Felt as “fluttering” or a “heavy” heartbeat

A

PACs

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79
Q

Precipitating factor of PACs

A

excess caffeine, stress, alcohol, nicotine, rec. drugs, hyperthyroidism

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80
Q

Often occur at rest

A

PACs

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81
Q

PACs on EKG:

A

Abnormal early P wave

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82
Q

Mobitz Type I Wenckebach

Caused by

A

intermittent failure of AV conduction

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83
Q

Progressive prolongation of PR until a QRS is dropped

A

Mobitz Type I Wenckebach

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84
Q

No PR prolongation, Sudden QRS drop

A

Mobitz Type II

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85
Q

More dangerous Mobitz

A

Type II

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86
Q

Mobitz Type I
• Typically
• If symptomatic (2 meds)

A

no treatment is required

IV ATROPINE or ISOPROTERENOL usually improves AV conduction

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87
Q

If Mobitz type I persists

A

Permanent pacemaker

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88
Q

Mobitz Type II interventions:

A

Cardiac Pacing (transcutaneous or transvenous)

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89
Q

Pacemaker warranted, even if pt. is asymptomatic, Mobitz

A

Type II

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90
Q

Causes of Tachycardia (FI 3H, CIA)

A 
Fever
Infection
Hypoxemia,hypovolemia, hyperthyroidism, 
CHF
Ischemia
Anemia
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91
Q

Usually from ↑ sympathetic tone and/or ↓ vagal EKG: normal waves, but rate >100

A

Sinus tachycardia

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92
Q

Sinus tachycardia rate

A

100-180 bpm

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93
Q

The most common manifestation of ischemic heart

disease

A

Angina Pectoris

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94
Q

Angina Pectoris caused by

A

Caused by imbalance of O2 supply & demand

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95
Q

Three forms of angina

A

Stable – Variant – Unstable

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96
Q

What type of angina is Relieved by rest (within a few minutes)

A

Stable

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97
Q

Stable angina on EKG shows

A

EKG: temporary ST Depressio

98
Q

What type of angina is precipitated by physical activity / emotional stress

A

Stable

99
Q

Transient type of angina

A

Stable

100
Q

What type of angina leads to Pain at rest

”

A

Variant

101
Q

Variant angina MAIN cause

A

Caused by spasm, not ↑O2 demand

102
Q

For Variant angina on EKG:

A

ST elevation

103
Q

a.k.a. “Prinzmetal Angina

A

Variant

104
Q

Unstable angina pain is

A

Increased frequency & duration of Pain at Rest

105
Q

Complications of Unstable angina pain

A

High risk of progression to MI if untreated

106
Q

For unstable angina on EKG

A

ST depression

107
Q

Evolution of Plaque (8 steps of formation)

A
  1. Various stressors cause endothelial dysfunction
    - allows entry of lipids into subendothelial space
    2&3. Oxidized lipids cause cytokine release from
    endothelium = chemoattractant for monocytes
  2. Monocytes take in lipids, become foam cells
  3. Impaired foam cells produce superoxide anion O2-
    and mmp (matrix metalloproteinases)
  4. Smooth muscle cells migrate into intima
  5. Muscle cells divide and produce matrix, enlarging
    plaque
  6. Some muscle cells undergo apoptosis, fibrofatty
    lesion forms, lipid core with fibrous fibrous cap
108
Q

Smooth muscle cells – Synthesize vasoactive inflammatory mediators:

A
  • IL-6

* TNF- α

109
Q

3 functions of Smooth muscle cells (VIPP)

A

–Produce extra cellular matrix
–Vasoconstriction/dilation
–Promote leukocyte proliferation
–Induce endothelial expression of LAM (leukocyte adhesion molecule

110
Q

Complications of Atherosclerosis

A

Calcification
Rupture/ulceration of plaque
Transmural Hemorrhage

111
Q

Complications of Atherosclerosis:Calcification

A

Imparts rigidity,↓ elasticity, ↑ fragility

112
Q

Complications of Atherosclerosis:Rupture/ulceration of plaque

A

Leads to thrombus, occlusion, infarct

113
Q

Complications of Atherosclerosis; Transmural Hemorrhage (FHC)

A

– From Microvessel growth within plaques
– Hematoma further occludes vessel
– Can cause rupture

114
Q

Plaque Stability :Inflammatory cytokines stimulate

A

foam cells to secrete MMP

115
Q

MMP role

A

Breaks down collagen & elastin

Weakens fibrous cap predisposing it to rupture

116
Q

Other complications Complications of Atherosclerosis

A

Embolization
Aneurysm –>Plaques weaken wall
Angina
MI

117
Q 
Mitral Stenosis (“MS”)
• Primarily affects M/F
A

Females

118
Q

Almost always rheumatic in origin

A

Mitral Stenosis (“MS”)

119
Q

For patients with MS they have hx of

A

50% of “MS” pts. have pos. Hx. ARF ~ 20 yrs. prior

120
Q

MS in Elderly pt.s – can be caused by

A

Calcification of valve

121
Q

MS congenital?

A

Congenital (rare)

122
Q

Pathologic features of MS:

A

– Fibrous thickening and calcification of valve leaflets
– Fusion of commissures
– Thickening & shortening of chordae tendineae

123
Q

Normal valve orifice of Mitral

A

4-6 cm^2

124
Q

Pathologic valve orifice in Mitral

A

< 2 cm^2

125
Q

Mitral Regurgitation Pathology

A

• Valve fails to close = ↓ SV and C.O.

126
Q

In MR, there is ____overload can lead to

A

LA; pulmonary congestion if acute

127
Q

MR is a structural abnormalities in the

A

annulus, leaflets, chordae tendineae, papillary muscle

128
Q

What is MVP?

A

Billowing of leaflets into LA w/ or w/o regurgitation

129
Q

What is the most common form of Valvular HD?

A

MVP

130
Q

Often asymptomatic; More common in women

A

MVP

131
Q

Valve recommended for elderly patients

A

Biologic

132
Q

How long does the biologic valve last____advantage (2):

A

8-10 years; NO AC, no clicks

133
Q

Valve Recommended for young pts.

A

Mechanical

134
Q

How long does the Mechanical valve last____advantage (2):

A

> 20 years

Anticoagulation needed, Click

135
Q

↑risk of _____ for all type valve replacements

A

endocarditis

136
Q

Fetal Circulation has 3 shunts:

A
  • Ductus venosus
  • Foramen ovale
  • Ductus arteriosus
137
Q

BP (bypass) lungs shunt

A

Foramen Ovale

138
Q

BP(bypass) liver shunt

A

Ductus Venosus

139
Q

Fetal Circulation blood path (UDIRFLA)

A 
Umbilical Vein
Ductus Venosus (BP liver)
IVC
RA
Foramen Ovale (BP lungs)
LA
Aorta
140
Q

Transitional Circulation:: What maintains PDA?

A

During fetal life, high levels of PGE-1 maintain PDA

141
Q

After birth what happens to

A

PGE 1 levels decline DA constricts closed

142
Q

Responsiveness to vasoactive substances is

A

age dependent

143
Q

With anatomic separation of circulatory paths,

Stroke volume of LV___ and RV ___

A

↑ ; ↓

144
Q

ASD Can occur anywhere along atrial septum, most

common

A

@ Foramen Ovale (failed fusion)

145
Q

PFO present in __%

A

~20% of the population

146
Q

When does the R-to-L shunt occur?

A

If RA press. ↑ 2o Pulm. HTN or RHF

147
Q

Termed “paradoxical embolism

A

PFO with R-to-L shunt can result in systemic embolism

148
Q

Explain paradoxical embolism

A

Embolus from systemic vein travels to RA, passes

across PFO to LA into systemic arterial circulation

149
Q

Tetralogy of Fallot Four anomalies:

A
  1. VSD
  2. Pulmonic Stenosis
  3. Aorta from both ventricles
  4. RV Hypertrophy
150
Q

Tetralogy of Fallot is a ______shunt

A

Right-to-Left shunt

151
Q

Aneurysm:

A

abnormal localized dilation

152
Q

In aneurysm, what happens to the diameter?

A

diameter increase of at least 50%

153
Q

“True aneurysm” =

A

dilatation of all three wall layers

154
Q

“True aneurysm” = 2 types

A

fusiform or saccular

155
Q

Fusiform –

. –

A

more common – symmetrical dilation of entire circumference of a segment

156
Q

Saccular aneurysm –

A

localized outpouching involving on a portion of the circumference

157
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

158
Q

Develop at sites of vessel injury:

A

infection – trauma – puncture of vessel during surgery or percutaneous catheterization – Very unstable, prone to complete rupture

159
Q

Majority of Aneurysms involve

•

A

Ascending thoracic aorta 65%
• Descending thoracic aorta 20%
• Aortic arch 10%
• Abdominal aorta 5%

160
Q

Aortic dissection classified as

A

Commonly classified as Type A or Type B

161
Q

Aortic Dissection

A

Immediate DX necessary with Contrast CT (CTA),

TEE, MRA or Constrast A-gram

162
Q

Coarctation of the Aorta Symptoms:
– Claudication in lower extremities following exercise
•

A

• HF if severe

163
Q

Coarctation of the Aorta: Differential Cyanosis if PDA present

A

– Upper half of body perfused; lower half cyanotic

164
Q

Coarctation of the Aorta• If less severe:

A

Claudication in lower extremities following exercise

165
Q

If Asymptomatic, coarctation suspected 2o to

• Treatment: Surgical correction

A

upper extremity HTN later in life

166
Q

Treatment of Coarctation of the aorta

A

Surgical Treatment

167
Q

Virchow’s Triad: Factors that predispose to

Venous thrombosis

A

Stasis of blood flow
Hypercoagulable states
Vascular damage

168
Q

Ex. Dental procedures or IVDA

A

Endocarditis

169
Q

90% of endocarditis cases are

A

G(+)

170
Q

Infected vegetations are source of

A

continuous bacteremia

171
Q

Thrombotic or septic emboli –

A

Infarct target organs (or vasa vasorum causing aortic

aneurysm)

172
Q

Antigen-Antibody complex deposition –

A

Glomerulonephritis, arthritis, vasculitis

173
Q

• Erosion into conduction system –

A

Manifest as heart block or other new arrhythmias

174
Q

• Acute Bacterial Endocarditis (ABE)

A
  • Fulminant infection
  • Highly virulent AND invasive
  • Staph aureus usual causative organism
  • May occur on previously healthy valves
175
Q

Subacute Bacterial Endocarditis (SBE)- LSO

A

• Less virulent
• Strep viridans usual causative organism
• Often occurs in pts. w/ prior underlying valve
damage

176
Q

• Staph epidermidis commonly causes

A

prosthetic valve endocarditis; (rarely on a native valve)

177
Q

IVDA often involves

A

right-sided heart valves

178
Q

Ventricular Hypertrophy and Remodeling

However, hypertrophied wall =

A

↑ stiffness, causes ↑ diastolic pressures, translated back to atria and pulmonary vasculature.

179
Q

• Pattern of remodeling depends on whether ventricle subjected to

A

chronic volume or pressure overload.

180
Q

Volume overload causes “eccentric hypertrophy”

A

– Results in synthesis of new sarcomeres in series with the old, causing myocytes to enlongate.
– Chamber radius enlarges in proportion to wall thickness.

181
Q

• Pressure overload causes “concentric hypertrophy

”

A

– Results in synthesis of new sarcomeres in parallel with the old, causing myocytes to thicken instead of elongate.
–

182
Q

Wall thickness increases without proportional chamber dilation = substantially ↓ wall stress.

A

Pressure overload “concentric hypertrophY”

183
Q

Effects of ↑ Preload

A

↑ SV, but constant ESV

184
Q

Effects of↑ Afterload result in

ESV, SV, EDV, ventricular pressure

A

↑ Ventricular pressure
↑ ESV
↓ SV
EDV remains constant

185
Q

Primary glomerulonephritis: 4 conditionw

A

– Minimal change disease (MCD)
– Focal segmental glomerulosclerosis (FSGS)
– Membranous glomerulonephritis (MGN)
– Membranoproliferative glomerulonephritis (MPGN)

186
Q

Minimal change disease (MCD

A

• Most common cause of nephrotic syndrome in children

187
Q

Focal segmental glomerulosclerosis (FSGS)

A

Most common cause of nephrotic syndrome in adults

188
Q

Membranous glomerulonephritis (MGN)

A

• Antibodies bind to basement membrane

189
Q

Membranoproliferative glomerulonephritis (MPGN)

A

• Damage to mesangium

190
Q

Post-streptococcal glomerulonephritis

• Anti-streptococcal antibodies

A

– antigen-antibody complexes deposit in glomeruli
– Activate complement MAC = vessel damage
– Increased capillary permeability – leakage of protein and large numbers of erythrocytes

191
Q

Treatment of post streptococcal glomerulonephritis

A

• Tx: BP meds, Diuretics, ABX if needed

192
Q

well-defined rounded deposits of immune

complexes outside capillary walls appear as humps

A

Post Streptococcal glomerulonephritis

193
Q

Renal Vein Entrapment Syndrome

a.k.a.

A

“nutcracker syndrome” due to similarity of

vessel position to a nutcracker:

194
Q

Renal vein Entrapment syndrome involves

A

– Aorta
– Superior Mesenteric Artery
– Renal Vein

195
Q

In renal vein entrapment

A

Venous hypertension causes rupture of thin-walled
veins into the collecting system with resultant
hematuria.

196
Q

Four Types of stones: –

A

Calcium oxalate (70%)
Uric acid (15%)
Struvite (15%)
Cystine (~1%)

197
Q

• Most common type of stone

A

Calcium oxalate

198
Q

Uric acid associated with

A

High purines

199
Q

Struvite stone associated with

A

Infection with ↑ pH

200
Q

Cystine associated with

A

Genetic disorder

201
Q

Uric acid is a by-product of

A

purine metabolism via xanthine oxidase pathway

202
Q

Normal uric acid in BLOOD is

A

2-7 mg/dl (blood);

203
Q

Normal uric acid in Urine

A

600 mg/dl

204
Q

95% people with ↑ uric acid are

A

asymptomatic

205
Q

High levels of uric acid due to 2 things

A

– Decreased excretion (90%)

– Over production (10%)

206
Q

Necrotic cells produce “muddy brown casts

A

Acute Tubular Necrosis (ATN)

207
Q

Most common cause of ARF (AKI)

A

Acute Tubular Necrosis (ATN)

208
Q

Classified as Toxic or Ischemic

A

Acute Tubular Necrosis (ATN)

209
Q

Tx: ATN

A

Treat underlying cause
Hydration
Stop offending drug

210
Q

Drugs/Toxins that cause ATN: CAMASREH

A 
Cisplatin
Aminoglycosides
Methotrexate – 
Amphotericin B
Statins 
Radiographic contrast 
Ethylene glycol 
Heavy metals
211
Q

Toxic ATN Involves

A

PCT only- casts form downstream of necrosis

212
Q

IgA Nephropathy

• a.k.a.

A

Berger’s Disease

213
Q

Most common cause of Nephritic Syndrome worldwide

A

IgA Nephropathy

• a.k.a. “Berger’s Disease

214
Q

Genetic predisposition to form Abnormal IgA after a

A

triggering event (ie. Infx or other allergin)

215
Q

IgA Nephropathy

• a.k.a. Bergers Pathophysiology

A

Abnormal IgA binds mesangium of glomerulus activating complement MAC damaging vessel wall

216
Q

• “Cola” colored hematuria

A

IgA Nephropathy • a.k.a. Bergers

217
Q

What is Fibromuscular Dysplasia

A

• Fibrous or fibromuscular thickening of artery wall

218
Q

Fibromuscular dysplagia shows alternating

A

Alternating pattern of stenosis and neurysms causes

“string of beads” appearance:

219
Q

3 types of Fibromuscular dysplagia

A

• 3 types:
– Intimal “focal”
– Medial “multi-focal” most common
– Adventitial

220
Q

Fibromuscular Dysplasia
• Multiple factors contribute to development:
GEMESOM

A 
Genetic
Estrogen
Mechanical stress
Environmental factors
Smoking
↓ Oxygen supply
Hormone
221
Q

Goodpasture’s Syndrome

A
  • Autoimmune disorder

* Antibodies attack basement membrane of Kidney and Lung

222
Q

Causes hemoptysis and hematuria

A

Goodpasture’s Syndrome

223
Q

• Causes of Good pasture syndrome

A 
– exposure to organic phosphates
– metal dust inhalation
– certain gene mutations HLA-DR15
– treatment w/ monoclonal
antibodies
224
Q

Henoch–Schönlein purpura

• a.k.a. “IgA Vasculitis” USUALLY IS

A

Usually self-limiting

225
Q

• Common cause of nephritic syndrome in children

A

Henoch–Schönlein purpura

a.k.a. “IgA Vasculitis”

226
Q

Malignant Nephrosclerosis
• a.k.a. “
QUICK or slow process

A

Hypertensive Nephrosclerosis”

Process occurs very quickly

227
Q

Vessel walls lose elastic fibers, become fragile,

rupture easily

A

Malignant Nephrosclerosis

228
Q

In Malignant Nephrosclerosis, you see

A
  • Pinpoint hemorrhages seen throughout kidney

* 2o to malignant HTN• (ex. 180/120 mmHg)

229
Q

GLOMERULONEPHRITIS

A

Inflammation of the glomerulus leads to ↑permeability and dysfunction

230
Q

Nephrotic syndrome:

A

proteinuria

231
Q

Nephritic syndrome:

A

proteinuria and hematuria

232
Q

GLOMERULONEPHRITIS

Causes include

A

both infectious and non-infectious processes.

233
Q

Urine protein normally

A

60-100 mg/day

234
Q

Urine protein >______ = Nephrotic Syndrome

A

3.5 g/day

235
Q

Nephrotic syndrome is characterized by:

A
  • massive Proteinuria
  • HYPOalbuminemia
  • Anasarca (Usually begins in the face)
236
Q

Nephrotic Syndrome

There is Hyperlipidemia why?

A

– Liver increases lipoprotein production in response to low plasma proteins

237
Q

Nephrotic Syndrome• Hyponatremia (dilutional)

A

Occurs with low fractional sodium excretion

238
Q

Nephrotic Syndrome Thrombophilia

A

– Due to loss of Antithrombin III in the urine

239
Q

Nephrotic syndrome other signs

A

Pitting edema
Pleural effusion
Muehrcke’s nails

240
Q

Scleroderma Renal Crisis (SRC)

A

uncontrolled accumulation of collagen and widespread vascular lesions

241
Q

Scleroderma Renal Crisis (SRC) causes

A

Causes thickening of the vascular wall and narrowing of lumen

242
Q

Arteries thickened in SRC

A

Intimal thickening of the interlobular and arcuate arteries

SRNAAnatomy II (16 decks)

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