Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

BMS200 > test 2 key part 2 > Flashcards

test 2 key part 2 Flashcards

1
Q

factors for hypertension

A

SNS activation, vasoconstriction, increase Na+ and renin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

hypertension mechanism

A
  • Increased resistance and tone, hypertrophy and hyperplasia of smooth muscle, arteriosclerosis, deposit ECM, release less vasodilatory NO
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

kidneys in hypertesnion

A
  • Kidneys: become hyperreactive to vasoactive stimuli, arteriosclerosis
  • Increased pressure in kidneys  increased salt and water loss (takes higher pressures to attain same level of salt loss)
    o Most arterioles constrict in response to increase pressure to reduce flow
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

The resetting of baroreceptors in hypertension does what

A

; for a given BP there is increased SNS activation
o Alpha 1 receptors; vasoconstrict
o ADH release; water retention
o Renin and AT II release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

leukocytes migrate into kidneys and vascular walls; activated by what in hypertension

A

o Activated by increased extracellular Na+
o Th17 cells and ILC3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

2 main causes of secondary hypertesnion

A

kidneys or SNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

hypertension diagnosis

A
  • Need multiple visits to diagnose unless >180/110 mm Hg
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

hypertensive urgency

A

elevated BP to treat urgently to minimize likelihood of end organ damage (i.e. stroke, IHD)

systolic >180 or diastolic >120

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

hypertensive emergency

A

hypertension with signs/symptoms that suggest end organ damage
o i.e. blurry vision, headache, stroke, angina, polyuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

malignant hypertension

A

> 180/120, end organ damage (hypertensive emergency), fibrinoid necrosis, hyperplastic arteriosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

difference between hypertensive urgency and emergency

A

urgency has bp of systole >180 or disstole >120 but no end organ damage

emergency has end organ damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

ca2+ channel blocker for hypertension

A

o Smooth muscle relax and dilate, negative dromotropy and chronotropy
o Could cause heart block or heart failure (from dromo and chrono)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

ACE inhibitors for hypertension

A

AT1 –> AT II inhibited
o Less aldosterone = less Na+
o Increase bradykinin: Vasodilate, NO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

angiotensin II (ARB) blockers for hypertension

A

o Block AT1 receptors = dilate and block aldosterone secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

alpha receptor blockers block what in hypertension and effect

A

(NE and E)
o Lower BP and peripheral resistance
o Adverse: reflex tachycardia, postural hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

vasculitis

A

Inflammation and necrosis of blood vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

primary vasculitis vs secondary vasculitis

A
  • Primary vasculitis = no underlying disorder
  • Secondary vasculitis i.e. medications, autoimmune (lupus, RA), infection (hepatitis B and C)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what T cells are activated in vasculitis

A
  • T lymphocyte activation and form granulomas
    o T helper cell (TH1/TH17) and giant cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what type of hypersensitivity reaction is vasculitis

A
  • Type III hypersensitivity (immune complex formation) complement activation, polymorphonuclear leukocyte (PMN) damages tissue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what antibodies are in vasculitis

A
  • Anti-neutrophil cytoplasmic antibodies ANCAa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

2 types of ANCAs

A

o P-ANCA in neutrophil nucleus; bind myeloperoxidase
o C-ANCA in cytoplasm; bind proteinase 3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

where are p-ANCA? where do they bind?

A

P-ANCA in neutrophil nucleus; bind myeloperoxidase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

where are c-ANCA? where do they bind?

A

C-ANCA in cytoplasm; bind proteinase 3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

how are neutrophils in vasculitis activated

A

o Neutrophil activation  express myeloperoxiade/proteinase 3 on cytoplasm  antibody binds and increase neutrophil and cytokines  endothelial damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

ANCA antigens are usually found _____ but in infection and inflammation they increase expression on _______

A
  • ANCA antigens usually in neutrophil cytoplasm but in infection and inflammation they increase expression on cell surface
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

temporal arteritis affects which artery

A

large arteies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

polyarteritis nodosa affects which arteries

A

small and medium arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

thromboangitis obliterans affects which arteries

A

small and medium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

granulomatosis with polyangitis affects which vessels

A

small and medium sized arteries and veins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what is the most common cause of vasculitis in elders

A

temporal arteritisi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

how to diagnose temporal arteritis

A

ESR/CRP and ultrasound of temporal artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

treatment of temporal ateritis

A

glucocorticoids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

cause of temporal arteritis

A

HLA-DR4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

symptoms of temporal arteritis

A

temporal headache
-scalp tenderness
-tongue and jaw claudication
-eyes ; vision loss, double vission
-fever, fatigue, polymyalgia rheymatica (pain in proximal muscles i.e. hip and shoudler)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

pathophysiology of temporal arteritis

A

-patchy granulomatous inflammation with giant cells and t cells
-usually carotid artery branches in temporal and opthalamic arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

polyarteritis nodosa affects many organs but rarely the

A

lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

pathophys of polyarteritis nodosa

A

patchy vessel
-neutrophils – fibrinoid necrosis
-thrombosis  infarct or aneurysm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

which organs is polyarteritis nodosa most common in

A
  • kidney (renal failure, hypertension)
    -MSK (arthritis, myalgia)
    -peripheral neuropathies (mononeuritis multiplex)

Minority is bowel infarct, areursym, CNS bleed, cholecystitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

skin symptoms in polyarteritis nodosa

A

purpura, nodule, raynauds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

cause of polyarteritis nodosa

A

HEP B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

diagnosis of polyarteritis nodosa

A

angiogram, CRP, neutrophils, hypergammaglobulinemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

thromboangitis obliterans

A

In distal legs and arms  occlusion and ischemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

who is htromboangitis obliterans common in

A

men, smokers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

symptoms in thromboangitis obliterans

A

-claudication, ulcers on hands and toes

-smoking; abnormal vasodilation
-neutrophils  thrombus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

diagnosis for Granulomatosis with polyangiitis

A

c-ANCA and biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

symptoms in Granulomatosis with polyangiitis

A

flaring disease
-fatigue, arthralgia, weight loss
-sinus pain and discharge, hemoptysis, dyspnea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

common sites for Granulomatosis with polyangiitis

A

kidney (glomerulonephritis), URT (sinusitis, otitis(, LRT (pulmonary infiltrate, pleuritis)
- skin and eye lesions and neuropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

pathophys of Granulomatosis with polyangiitis

A

-necrotizing vasculitis with intravascular or extravascular granuloma formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

raynauds

A
  • Intermittent bilateral asymmetric ischemia of fingers and toes
  • Caused by transient vasospasm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

what is raynauds usually in

A
  • Usually in immunologic disorders (lupus)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

what makes raynauds worse

A

cold and stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

raynauds progression

A

Digits first turn white (vasoconstriction), then blue (cyanosis), then bright red (hyperemia) when blood flow is restored

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

ECG lead placement

A
  • Coronal view (left and right arms, left leg)
  • Cross sectional view (precordial leads)
  • Bipolar leads: compare voltage changes between leads (i.e. leg and arm)
  • Unipolar (precordial leads): compare voltage changes between lead (surface of chest) and center of heart
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

how to determine rate in an ECG

A

a. Divide 300 by number of large boxes between R-waves (R-R interval) = rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

what is a normal sinus rhythm

A

pacemaker is SA node, no abnormal conduction
i. Regular or regularly irregular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

findings in normal sinus rhythm

A

ii. Each p wave is followed by QRS (<100ms, 2.5 small boxes), PR interval is constant
iii. Each QRS complex is followed by P wave

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

regularly irregular

A

can be normal; HR varies with respiration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

irregularly irregular

A

tachycardia, like atrial fibrillation and is abnormal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

intervals problems

A

widened or shortened?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

PR interval problem

A

usually prolongation = AV nodal dysfunction
i. Abnormal connection between atria and ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

QRS interval problem

A

delay in ventricular excitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

QT interval problem

A

repolarization abnormalities (torsades de pointes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

normal QRS, QT, PR

A

e. Normal QRS= normal interventricular conduction pathways
f. Normal QT= normal ventricular repolarization
g. Normal PR= no abnormal delays/ consuctions at AV node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

QT interval varies with

A

heart rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

how to finds QT corrected

A

i. QT corrected = QT / square root of (R-R interval)
ii. If less than half of R-R is usually good

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

ST segment isn’t looked at under interval category its under

A

waves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

abnormal Q wave

A

current or prior MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

ST segmenet elevation or depression?

A

rule out infarct

depression: NSTEMI, digoxin, hypokalmeia, RVH, LVH, RBBB, etc

elevation: STEMI, pericarditis, LBBB, LVH, hyperkalemia, raised intracranial pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

T waves normal and problem

A
  • should be upright in all leads except V1
    i. Tall: hyperkalemia, early MI
    ii. Small: hypokalemia
    iii. Inverted: MI, ventricular hypertrophy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

P waves problems

A

i. Change beat to beat= pacemaker not the same
ii. Absence- atrial fibrillation
iii. More P waves than QRS complexes= heart block

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

3 types of general pathophysiology of dysrhythmias

A
  1. re-entry
  2. ectopic foci or abnormal automaticity
  3. triggered activity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

re=entry

A

a. Normal depolarization wave enters a pathological space in the heart; contraction can’t occur but may allow slower conduction of wave to healthy tissue
b. Healthy tissue completes refractory period

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

re-entry causes

A

tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

areas with XX cause re-entry

A

d. Area with a block slowing conduction OR conditions that slow refractory period cause re-entry (i.e. atrial fibrillation, atrial flutter, paroxysmal supra ventricular tachycardia, premature ventricular contraction)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

ectopic foci

A

Scar tissue changes local plasma electrolyte concentrations or their movements across channels resulting in occurrence of automaticity in previously non pacemaker cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

what is inhibited in ectopic foci

A

i. Inhibit Na/K pump causes accumulation of Na and Ca which partially depolarizes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

automaticity in previously non pacemaker cells from changes in electrolyte concentration or channel movement from scar tissue

A

ectopic foci

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

abnormal automaticity

A

i. Decrease K+ conductance at rest (catecholamines, hyperkalemia, hypercalcemia)
ii. Increase intracellular Ca2+
iii. Cardiac metabolism; IR K+ channels inactivated by intracellular ATP, activated by ADP allowing K+ efflux and reduced refractory period

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

what is triggered activity

A

a. Ventricular arrhythmia; normal AP followed by abnormal depolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

what causes triggered activity (ventricular arrhythmia; normal AP followed by abnormal depolarization)

A

i. Premature ventricular contractions
ii. Bradycardia and reduced or prolonged phase 3
iii. Tachycardia and increases Ca2+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

chronic inflammation from

A

fibrosis via cytokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

what do cardiac fibroblasts turn into in fibrosis and via what?

A
  • Cardiac fibroblasts turn into myofibroblasts via AT II, aldosterone, catecholamines, TGF beta, inflammatory cytokines, ROS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

cardiac fibroblast vs myofibroblasts in firborisi

A
  • Myofibroblasts produce more ECM and cause fibrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

fibrosis leads to

A

remodelling of myocardial collagen
o Local delay in portion of the heart
o Promotes re-entry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

fibrosis promotes

A

re-entry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

what is the most common arythmia

A

atrial fibrillation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

risks for atrial fibrilation

A

age, hypertension, alcohol, sleep apnea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

what happens when atrial fibrillation occurs

A

turbulent blood flow, reduce heart effectiveness, increased thrombus risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

symptoms of atrial fibrillation

A

asymptomatic OR chest pain, palpitations, tachycardia, dizzy, diaphoresis, fatigue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

pathophysiology of atrial fibrillation

A

atrial structure (ECM, fibrous tissue) and electrical (shorten refractory period, tachycardia) –> remodelling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

dysrhythmias in atrial fibrilation

A

ectopic foci
re entry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

prognossis of atrial fibrillation

A

leading cardiac cause of stroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

ECG in atrial fibrillation

A

narrow complex “irregular irregular” with no distinguishable p wave

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

symptoms of atrial flutter

A

fatigue, palpitation, syncope

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

what dysrhythmia in atrial flutter and pathophysiology

A

re entry due to fibrosis  fast and slow conductions AND different refractory period

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

ECG in atrial flutter

A

fast atrial rate >300bpm with fixed or variable ventricular rate

Flutter waves without an isoelectric line in between QRS complex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

sinus tachycardia effects on heart rate and cardiac output

A

Normal rhythm, heart beats faster and increased cardiac output

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

what can cause sinus tachycardia

A

From stress or exercise (catecholamines); concerning if at rest
(myocarditis or other cardiac or non cardiac like infection, pulmonary embolism, hypoglycemia, shock)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Paroxysmal supraventricular tachycardia is

A

Intermittent (paroxysmal) episodes of supraventricular tachycardia with sudden onset and stop

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

cause of Paroxysmal supraventricular tachycardia

A

hyperthyroid, coffee, cocaine, anxiety, heart disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

prognosis of Paroxysmal supraventricular tachycardia

A

ok unless heart disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

symptoms of Paroxysmal supraventricular tachycardia

A

dizzy, palpitations, nausea, anxiety

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

dyrhytmia in Paroxysmal supraventricular tachycardia

A

Re-entry  sometimes due to increased automaticity or trigger

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

ECG in Paroxysmal supraventricular tachycardia

A

-often narrow QRS complex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

where does the problem orginate in Paroxysmal supraventricular tachycardia

A

Originate from atria or AV nodes  regular or irregular rhythms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

what initiates the heart beat in Premature ventricular contraction

A

Heartbeat is initiated by Purkinje fibers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

is Premature ventricular contraction common?

A

yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

types of Premature ventricular contraction

A

isolate or double or triplet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

cause of Premature ventricular contraction

A

caffeine, excess catecholamines, anxiety, electrolyte imbalance, hyperthyroid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

symptoms in Premature ventricular contraction

A

-skipped heartbeat, chest pain, lightheaded, dyspnea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

prognosis of Premature ventricular contraction

A

ok unless heart disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

ECG in Premature ventricular contraction

A

Abnormal and wide QRS complex occurring earlier than expected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

dysrhythmia in Premature ventricular contraction

A

ectopic nodal automaticity
-re-entry
-triggered activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

what isn’t working in idioventricular rhythm

A

SA node (and AV) isn’t working, ventricle takes over

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

cause of idioventricular rhythm

A

heart block, electrolytes, medication, reperfusion after MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

symptoms in idioventricular rhythm

A

asymptomatic or palpitations, lightheaded, fatigue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

heart rate in idioventricular rhythm

A

Slow regular ventricular rhythm <50bpm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

ECG in idioventricular rhythm

A

P wave absent, prolonged/ wide QRS interval

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

common cause of ventricular tachycadia

A

Commonly from ischemic heart disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

preload and SV and cardiac output in ventricular tachycadia

A

Reduced preload and stroke volume leads to low cardiac ouput

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

symptoms in ventricular tachycadia

A

palpitations, chest pain, dyspnea, syncope, cardiac arrest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

prognosis of ventricular tachycadia

A

Potentially life threatening (hypoperfused  progress to ventricular fibrillation  cardiac death)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

heart rate in ventricular tachycardia

A

> 3 consecutive ventricular beats w rate of 100-250bpm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

ECG in ventricular tachycadia

A

wide QRS complex

Ventricular tachycardia causes a wide QRS complex because the impulse originates in the ventricles (instead of the atria or AV node) and spreads slowly through the ventricular myocardium rather than the specialized Purkinje fibers.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

dysthymia present in ventricular tachycadia

A

Re entry (most common)
-triggered activity and enhanced automaticity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

ventricular tachycarid

A

The abnormal electrical impulses originate from an ectopic focus within the ventricles, rather than from the sinoatrial (SA) node or the atrioventricular (AV) node.
The focus of the arrhythmia may be a scarred area (e.g., from previous myocardial infarction (MI)) or an area of electrical instability within the myocardium.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

ventricular fibrilation cause

A

From MI, electrolyte, alcohol, hypothermia, cardiomyopathies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

ventricular fibrillation presentation

A

Irregular electrical activity, ventricular rate >300bpm, reduced cardiac output  sudden cardiac death in minutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

symptoms in ventricular fibrilation

A

Chest pain, dyspnea, vomit, unconscious

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

ECG in ventricular fibrillation

A

No identifiable P wave, QRS complex, T wave, HR 150-500bpm,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

dysrhythmia in ventricular fibrillation

A

Increased automaticity of purkinge cells

Triggered acitivity

Possible re entry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

Torsades de pointes is a form of

A

ventricular tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

Torsades de pointes

A

Form of ventricular tachycardia  rhythm may terminate spontaneously or progress into ventricular fibrillation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

causes of Torsades de pointes

A

Congenital or acquired from meds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

which electrolyte in Torsades de pointes

A

Prolonged repolarization from delay in K+ efflux

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

symptoms of Torsades de pointes

A

Asymptomatic OR syncope, palpitation, dizzy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

10% of Torsades de pointes can result in

A

cardiac death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

QTc in Torsades de pointes

A

QTc prolongation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

ECG in Torsades de pointes

A

Twisting ECG, polymorphic, vary amplitude of QRS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

what differentiated ventricular tachycardia from other supraventicular arrhythmias

A

The wide QRS complex of Ventricular Tachycardia helps differentiate it from other supraventricular arrhythmias, which typically have narrow QRS complexes (because the impulse is conducted normally through the His-Purkinje system).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

what is a conduction block

A
  • Arrythmia caused by delay or complete block of heart, esp AV node or bundle branches
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

where are conduction blocks commonly found

A

AV NODE or bundle branches

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

conduction blocks lead to

A

inadequate HR, dizzy, fatigue, syncope

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

3 types of conduction block

A

-1st degree AV block
-2nd degree AV block
-3rd degree AV (complete heart block)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

first degree heart block cause

A

Caused by increased vagal tone or fibrotic changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

symptoms in first degree heart block

A

none

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

impulse conduction in first degree heart block

A

good- Every impulse conducted to the ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

PR interval in first degree heart block

A

Prolonged PR interval (slow conduction through AV node)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

second degree AV block symptoms in type 1 vs type 2

A

Type I: asymptomatic
Type II: bradycardia, cardiac arrest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

second degree AV block: type 1 vs type 2 ECG finidngs

A

Type i: prolonged PR interval until QRS complex is dropped
Type II: consistent PR interval with sudden drops of QRS (more serious – can progress to 3rd degree)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

cause of second degree AV block symptoms

A

High vagal tone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

third degree AV block effect on ECG and cardiac output

A

Cardiac output reduced

Regular P waves and QRS but no coordination between

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

third degree AV block impulse conduction?

A

No impulse from atria reaches the ventricles, independent atrial and ventricular rates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

third degree AV block symptoms

A

Bradycardia, syncope, heart failure; need pacemaker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

third degree AV block cause

A

Fibrosis or heart disease, electrolytes, meds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

cardiac ishcemia impat on ECG

A

inverted T wave

  • ST elevation in leads near injury
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q

4 classes of anti arrhythmic medications

A

Class 1 antiarrhythmic
- Bind Na+ and prevent influx
- Inhibit K+
- Block Ca2+
o Negative dromotropy (slow conduction) and increase refractoriness (interfere with Ca2+ repolarization)

Class 2 antiarrhythmic
- Beta blocker reduce phase 4 and HR and prolong AV conduction and reduce contractility
- Treat arrhythmias causes by increased SNS activity

Class 3 antiarrhythmic
- Block K+ channels reducing efflux and prolong AP and refractory period

Class 4 antiarrhythmic
- Block Ca2+ and reduce influx, phase 4, and spontaneous depolarization
- Slow down conduction
o Side effects: bradycardia, hypotension, peripheral edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

use of class 2 antiarrhytmic med

A

beta blockere

  • Treat arrhythmias causes by increased SNS activity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q

which sleep is most important for cognitive performance

A

N3 deep sleep

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q

which sleep has less psychologic consequences

A

REM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

polysomnography for sleep study 4 parts

E_G

A
  • EMG (electromyogram) – face and leg muscle
  • EOG (electrooculogram)- eye movements
  • ECGs and pulse oximeters – oxygenation and cardiac function
  • EEG (electroencephalogram)- skull/ cortex
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
162
Q

EEG measures which cells

A

pyramidal cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
163
Q

EEG measure the difference in

A

o Measure difference in potential between dendrite and cell body; not directly measuring APs
o Measures frequency of potential (waves in Hz) and size of waves (uV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
164
Q

frequencies in EEG sleep

A

o Alpha= eyes closed and mind wanders- 8-13Hz, medium amplitude waves
o Beta= eyes open and wide awake- 13-30Hz, low amplitude waves
o REM and Awake= dys-synchronized /random patterns
o Alpha block/arousal/alerting response: when focused; decrease alpha wave

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
165
Q

what is alpha block/ alerting response

A

when focused; decrease alpha wave

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
166
Q

alpha is

A

eye closed and mind wanders, relaxed wakefullness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
167
Q

beta is

A

eyes open and wide awake, thinking, stressed

168
Q

theta is

A

drowsy, light sleep

169
Q

delta is

A

deep N3 sleep

170
Q

frequency in alpha, beta, theta and delta

A

Beta- 13-30Hz
Alpha- 8-13 Hz
Theta- 4-8 Hz
Delta- 0.5-4 Hz

171
Q

amplitude in 4 waves

A

Delta- high
Theta- med to high
Alpha- Med
beta- low to high

172
Q

N1 sleep

A

transition from wake to sleep

173
Q

which wave in N1 sleep

A

theta

174
Q

EMG and EOG in N1 sleep

A

rolling slow eye movements

175
Q

move in N1?

A

large axial muscle movements

176
Q

N2 slee

A

light sleep

177
Q

2 key findings in N2 sleep

A
  • K complexes – intermittent high amplitude spikes
  • Sleep spindles- 7-15Hz groups of waves
178
Q

eyes and legs in N2 sleep?

A
  • Limited to no eye movement
  • Large movements of axial muscles
179
Q

eyes and legs in N4 sleep

A
  • Minimal eye movement
  • Large movements of axial muscles
180
Q

eye movements in which sleep stages

A

N1 has rolling slow eyes

REm has rapid eyes

181
Q

which has axial limb movement and which sleeps tables dont

A

REM doesnt, other do

182
Q

N4 is

A

stage 3 and 4= deep sleep

183
Q

wave in N4 sleep

A

delta= low frequency, high amplitude
o Oscillations in activity between thalamus and cortex

184
Q

eyes and legs in N4 sleep?

A
  • Minimal eye movement
  • Large movements of axial muscles
185
Q

REM sleep EMG and EOG findings

A
  • Rapid eye movement on EOG
  • EMG flatline- no MSK movement
186
Q

wave in N1 and REM

A

theta

187
Q

wave in REM

A
  • Theta= Low amplitude, high frequency like N1 but lower amplitude and not synchronized
188
Q

which sleep stage do u remember dreams in

A

REM

189
Q

which sleep stage are u easily awakened in

A

REM

190
Q

what causes the few movements in REM

A
  • GABA to activate spinal inhibitory neurons  paralyzed, few movements
191
Q

which sleep period is the longest? how long?

A
  • 1st sleep period is the longest: 90-110 minutes
192
Q

which population gets most deep sleep? at what point in the night?

A
  • Kids/ young adults get most N3 deep sleep early, soon after falling asleep
193
Q

progression of sleep stages

A

N1,N2,N3, REM

194
Q

what sleep stage is last

A
  • Never go from wake to REM, its last
  • REM occurs near end of sleep session
195
Q

elders and sleep

A
  • Elders have less N3 and more awakenings
196
Q

arousal system; brain areas involved

A

open the gate of thalamus to allow input from outside world to cortex

o Communicates with hypothalamic areas

197
Q

brainstem nuclei in the arousal system

A

 Locus coeruleus- norepinephrine
 Raphe nucleus- serotonin
 Tuberomammillary body- histamine
 Acetylcholine- multiple brainstem nuclei
 Periaqueductal gray- dopamine

198
Q

locus coerulus- what neurotransmitter?

A

NE

199
Q

raphe nucleus- what neurotrasnmitter

A

serotonin

200
Q

tubermamillary body- which neurotransmitter

A

histamine

201
Q

where is acetylcholine found in the brainstem

A

multiple brainstem nuclei

202
Q

periaqueductal grey- which neurotransmitter

A

dopamine

203
Q

which part of the brain is sleep promoting

A

ventrolateral pre-optic nucleus VLPO

204
Q

what does the ventrolateral pre-optic nucleus VLPO release

A

galanin and gaba

205
Q

2 things that promote sleep

A

galanin and gaba

206
Q

what 2 things regulate REM

A

REM on and REM off

207
Q

where is REM off

A

pons

208
Q

where is REM on

A

lateral pontine

209
Q

what does SCN communicate with

A

o SCN communicates with retina for circadian rhythm via light dark

210
Q

what are the 2 stabilizing nuclei in the lateral hypothalamus that allow for stable sleep (or fully awake)

A
  1. orexin
  2. melanin concentrating hormone MCH
211
Q

orexin projects where?

A

– projects to arousal system and VLPO

inhibits VLPO and makes us awake

212
Q

melanin concentrating hormone MCH projects to where

A

aoursal system

inhibits it to make us sleepy

213
Q

orexin and melanin concentrating hormone where they project to

A

MCH to arousal system (inhibits it) = sleepy

orexin to arousal system and VLPO (inhibits VLPO) = awake

214
Q

what makes us sleepy (2)

A

o Homeostatic signal
o Circadian rhythm

215
Q

what wakes us

A

o Arousal system inhibits VLPO
o Orexin increases
o Orexin + inhibit VLPO = durable wake state

216
Q

what makes us sleepy

A

o VLPO activated
o Inhibit arousal and orexin
o MCH released during REM inhibits monoaminergic arousal system (i.e. dopamine, serotonin)

217
Q

where is melatonin made and stimulated by what?

A
  • Made in pineal gland in darkness
218
Q

which fibers work in the absence of light

A
  • In the absence of light→ retinohypothalamic fibres relay “dark info” to the SCN→ lifting of the inhibition of the PVN by the SCN

o Absence of light  PVN activates SNS  intermediolateral horn  excite superior cervical ganglion  release NE from pineal gland  make melatonin

219
Q

what is released by the pineal gland to make melatonin

A

NE

220
Q

which amino acid starts melatonin synthesis

A

tryptophan

221
Q

what does tryptophan become in melatonin path

A

serotonin

222
Q

how does serotonin become melatonin

A
  • Metabolite of serotonin (from tryptophan)
    o With catecholamine (NE) stimulation the activity and production of AANAT  make melatonin
     Withdrawal catecholamines = degrade AANAT by proteosomes
223
Q

which melatonin receptors are entrain SCN to 24 hour light dark cycle

A

MT-2

224
Q

MT1 vs MT2 melatonin receptors

A
  • Melatonin can decrease sleep latency (MT-1) and increase amount of sleep (MT-2)
225
Q

what else does melatonin entrain

A

core body temperature, HR variability, cortisol and TSH secretion

226
Q

what enzyme to turn serotonin into n-acetylserotonin then into melatonin

A

AANAT (rate limiting) (arylalkylamine n-acetyltransferase)

HIOMT

227
Q

what builds up if you go without sleep and helps with homeostatic drive

A

adenosine

228
Q

what is an adenosine receptor (A2a) antagonist

A

caffeine

229
Q

A1 and A2a adenosine receptors

A
  • A1 inhibit arousal, A2a facilitate sleep
230
Q

what is allostasis

A

response to stressors

o I.e. psychologic stress causes sleep problems -overactivated monoaminergic arousal system

231
Q

narcolepsy

A
  • Excessive daytime sleepiness
  • Intrusion of REM into wakefulness
232
Q

symptoms in narcolepsy

A
  • Cataplexy, sleep paralysis, dream like hallucinations while awake
233
Q

which neurons are lost in narcolepsy and cataplexy

A

orexigenic neurons

234
Q

what is the cause of loss of orexigenic neurons in cataplexy and narcolepsy

A

o Usually autoimmune
o Molecular mimicry of orexin from influenza and strept

235
Q

cataplexy

A

muscle weakness without loss of consciousness

236
Q

which type of narcolepsy has cataplexy

A

type I narcolepsy

237
Q

hypnagogic vs hypnopompic hallucinations

A
  • Hypnagogic hallucinations- sleep paralysis and hallucinations when falling asleep
  • Hypnopompic hallucinations- upon wakening
238
Q

sleep architecture in narcolepsy

A
  • Enter REM quickly at night, fragmented sleep, naps
239
Q

treatment of narcolepsy

A

antidepressants to increase NE or serotonin  stimulate REM off neurons
o methylphenidate or modafinil to increase dopamine at synapse

240
Q

restless leg syndrome vs periodic limb movement

A
  • RLS: compulsion to move legs that’s triggered by rest
  • PLMD: occurs during sleep- large movements of legs/ kicking, can occur with RLS
241
Q

causes of periodic limb movement disorder

A

o Iron deficiency – iron transport/metabolism
o Abnormal dopaminergic signaling in susbstantia nigra
o Treat: dopamine agonist (excess in AM and inadequate at PM)
o Movement disorders from basal ganglia and substantia nigra

242
Q

needed to diagnose OSA

A
  • 5+ episodes of OA or hypoapnea in 1 hour of sleep
243
Q

apnea vs hypopnea

A
  • Apnea= cessation of airflow for > 10 seconds
  • Hypoapnea= >30% reduction in airflow for at least 10 seconds with oxygen desaturation or waking
244
Q

severe OSA

A

> 15 episodes/hour

245
Q

symptoms in OSA

A
  • Gasp, snore, choke, awaken, daytime sleepiness, fatigue, morning headaches
246
Q

inspiration in OSA

A
  • Inspiration –> negative pressure in pharynx  collapse bc of decreases muscle tone in sleep
247
Q

which sleep stage is OSA most severe in

A

REM

248
Q

risk factors for OSA

A
  • Upper body adiposity, septal deviation, nasal polyps, small jaw, genes, male, diabetes, hypertension
249
Q

where should tongue go when mouth closed

A

seal to soft palate

250
Q

CO2 sensitivity in OSA

A
  • CO2 sensitivity  increase ventilatory drive  in OSA stiffens upper airway muscles  patent pharynx
251
Q

hypercarbia and OSA

A
  • Hypersensitive to hypercarbia  increase pharyngeal stiffness
252
Q

how to diagnose OSA

A

polysomnogrpahy

253
Q

parasomnia

A
  • Abnormal behaviours or experiences in sleep
254
Q

sleepwalking

A

automatic motor activity, mostly in N3 (early evening), mostly in kids

255
Q

which sleep stage for sleep walking

A

N3

256
Q

sleep terror in which sleep stage

A

N3

257
Q

sleep terrors

A

kids awaken screaming, N3, tachycardia, hyperventilate, sweat,

258
Q

how to avoid sleep walking and sleep terrors

A

ensure adequate sleep

259
Q

REM sleep behaviour disorder

A

act out dreams; kicking, punching, increases with age, usually develop neurodegenerative disorders

260
Q

what is the endoneurium in the PNS

A

CT encasing individual nerve fibers, contains blood vessels

261
Q

axon microtubular apparatus function in PNS

A
  • Transport NTs and structural support
262
Q

2 types of nerve fiber damage in PNS

A
  1. axonal degeneration
  2. segmental demyelination
263
Q

distal axon degeneration

A

distal portion of long nerve fibers; cell bodies and proximal axons unaffected

264
Q

wallerian degeneration

A

degeneration beyond where its compressed or severed. If close to origin can regenerate.

  • Deterioration of axis cylinder and myelin and central chromatolysis
265
Q

neuronopathy (type of axonal degeneration)

A

neuronal cell body and axon degenerated; i.e. autoimmune

266
Q

segmental demyelination

A

myelin sheath deteriorate, but underlying axon still functional

267
Q

primary vs secondary demyelination

A

o Primary demyelination: direct injury to schwann cell or myelin sheath
o Secondary demyelination: underlying axonal abnormalities

268
Q

what invades in segmental demyelination

A

o Macrophages invade and eliminate myelin debris

269
Q

functional recovery in segmental demyelination

A

degeneration followed by schwann cell proliferation then remyelination

 Remyelinated section have reduced internode lengths (less efficiencet)

270
Q

hypertrophic neuropathy (type of segmental demyelination)

A

repeated episodes of segmental peripheral nerve demyelination and remyelination – accumulation of supernumerary Schwan cells that encircle the axons (onion bulbs)

271
Q

PNS vs CNS

A

PNS fibers can regenerate and remyelinate

272
Q

is peripheral neuropathy typically axonal degeneration of segmental demyelination?

A
  • 90% axonal
    o If demyelinating its hereditary or immunological
273
Q

large vs small diameter fibers for what

A
  • Large diameter sensory fibers- proprioception and vibration
  • Small diameter myelinated and unmyelinated fibers- pain and temperature
274
Q

pain and temperature

A
  • Small diameter myelinated and unmyelinated fibers-
275
Q

proprioception and vibration

A
  • Large diameter sensory fibers
276
Q

main causes of peripheral neuropathy

A

DIABETES

: metabolic (diabetes, thyroid), nutritional (B12 deficient), systemic (HIV, lyme, hepatitis), toxic (alcohol, chemo)

277
Q

features of peripheral neuropathy

A

muscle weakness and atrophy, sensory loss, paresthesisa, pain, autonomic dysfunction

278
Q

polyneuropathy

A

weak symmetrical bilateral, lose reflexes in ankles, decreased sensation in distal extremities

279
Q

radiculipathy or polyradiculopathy

A

asymmetrical, sporadic distribution, weak, sensory loss, pain; nerve root distribution (compression of nerve root)

280
Q

mononeuropathy

A

weak and sensory loss in single peripheral nerve

281
Q

multiple mononeuropathies (mononeuropathy multiplex)

A

many mononeuropathies ; difficult to differentiate from polyneuropathy

282
Q

plexopathy (involvement of multiple nerves in a plexus)

A

brachial or lumbosacral plexus. Single limb impacted, but motor, sensory and reflex deficits don’t align with pattern of multiple nerves

283
Q

neuronopathy (motor or sensory) which cells effected?

A

ganglion cells effected  sensory deficits proximally and distally

284
Q

autonomic symptoms in peripheral neuropathy

A
  • Autonomic: impaired sweat, heat intolerance, bladder incontinence, BP not regulated, GI
285
Q

motor symptoms in peripheral neuropathy

A
  • Motor: weak, spasm, wasting, reflexes
286
Q

sensory symptoms in peripheral neuropathy

A

o Large fibers (with myelin): reduced sensation, reflexes, limb position

o Small fibers (no myelin sheath): compromised perception of pain and temperature

287
Q

what type of neuropathy is diabetic neuropathy?

A
  • Polyneuropathy: distal symmetric sensory or sensorimotor polyneuropathy, autonomic neuropathy, diabetic neuropathic cachexia, polyradiculoneuropathies, cranial neuropathies, and other mononeuropathies.
288
Q

risk for developing diabetic neuropathy

A

inadequate DM managing

289
Q

high blood sugar increae which pathway

A

polyol pathway

290
Q

what 2 sugars accumulate in nerves and damage them

A

fructose and sorbitol

291
Q

diabetic neuropathy pathophysiology

A
  • High blood sugar increases polyol pathway activity  accumulate fructose and sorbitol in nerves  damage
292
Q

blood glucose > XX affects polyol pathway

A

o Blood glucose >7 mmol/L augments glucose flow in polyol pathway

293
Q

what is the key regulating step in the polyol pathway to prevent diabetic neuropathy

A

Glucose –> sorbitol by aldose reductase and NADPH

294
Q

immune in diabetic neuropathy? what type of antibodies?

A

antineural autoantibodies, antiphospholipid antibodies = nerve damage and vascular irregularities

295
Q

why is there endoneural vascular insufficiency in diabetic neuropathy?

A
  • Endoneural vascular insufficiency from reduced NO and compromised Na+/K+ ATPase and elevated homocysteinemia  vascular permeability and hindered endoneural blood flow
296
Q

pattern in diabetic neuropathy

A
  • Stocking and glove pattern; sensory loss, dysesthesia, painful paresthesia, lower limbs
297
Q

symptoms in diabetic neuropathy

A
  • Tingle, prick, numb, burn or freeze, sharp pain, sensitive to touch, muscle weak
298
Q

increaed oxidative stress in diabetic neuropathy does what

A

increased AGES advanced gylcation end products

299
Q

increased sorbitol in diabetic neuropathy does what

A

decreased Na+/K+ ATPase activity and decreases free carnitine and myoinostiol

300
Q

____ nitric oxide and ____ homocysteine in diabetic neuropathy impaired endothelial function

A

decreased NO and increases HC

301
Q

what causes cobalamin (B12) deficiency

A

pernicious anemia

o Also vegetarian, by-pass surgery, IBD, pancreatic insufficiency, PPIs…

302
Q

vitamin B12 deficiency neuropathy is

A
  • Autoimmune antibodies target parietal cells and intrinsic factor
303
Q

autoimmune antiboedies in B12 deficiency neuropathy target what 2 things

A

intrisnci factor and parietal cells

304
Q

what helps with digestion is decreased in vitmain B12 defiiency neuronopathy

A
  • Atrophic gastritis, achlohydria (no gastric acid secretion)
305
Q

neurological symptoms in vitmain B12 defiiency neuronopathy

A

peripheral neuropathy and cognitive

306
Q

what does B12 play a role in

A
  • B12 role in 1 carbon cycle: coenzyme for methionine synthesis; needed for RNA and DNA production
307
Q

B12 is needed for

A

DNA and RNA synthesis

308
Q

B12 is a coenzyme for

A

methionine sysnthesis

309
Q

B12 defiicency causes the accumulation of what

A

homocysteine accuualtes (because u need b12 to turn homocysteine in methionine)

310
Q

B12 impacts ___ metabolism

A

folate metabolism

311
Q

B12 converts _____ into _______ which is needed for myelin sysntehsis and stability

A

methylmalonyl CoA into succinyl CoA

312
Q

if b12 defienct and cant turn methylmalonyl CoA into succinyl CoA what happens to myelin

A

abnormal fatty acids and demyelinate

313
Q

what type of neuropathy is b12 defieicny ; axonal or demyleianting

A
  • Majority have axonal involved, some have demyelinating changes
314
Q

symptoms in b12 deficiency neuropathy

A

numb hands 1st then progress to paresthesia in lower extremities
o Hyperreflexia, unsteady gait, no Achilles reflex

315
Q

which fibers are impacted and which are spared in b12 deficient neuropathy

A
  • Impact large fibers; proprioception and vibration
    o Small fibers are spared
316
Q

symptoms in chemotherapy induced peripheral neuropathy ? which axons affected?

A
  • Glove and stocking, affects longer axons
317
Q

changes in chemotherpay induced peripheral neuropathy

A
  • disturbances in microtubules, oxidative stress-induced mitochondrial damage, changes in ion channel function, injury to the myelin sheath, DNA damage, immunological responses, and neuroinflammation
318
Q

chemotherpay induced peripheral neuroapthy is dose dependent; what is effecting the tissu e

A

platinum

319
Q

which chemo meds in peripheral neuropathy

A
  • paclitaxel and docetaxel for ovarian cancer cause neurotubule depolymerization
320
Q

hypothyroidism is what type of peripheral neuropathy

A

proximal myopathy

321
Q

hypothyroid changes that cause peripheral neuropathy

A

mucopolysaccharides, chondroitin sulfate and hyaluronic acid accumulate in interstitial spaces= water retention and weight gain and compress nerves

322
Q

carpal tunnel is common in

A

hypothyroid induced peripheral neroopathy

323
Q

weight gain in hypothroid effects

A

nerve conduction

324
Q

hypothyroid has energy defiecient from nutrient oxidation; how does it cause neuropathy

A

; less ATP and Na+/K+ pump and accumulation of glycogen deposits can cause neuropathy

325
Q

changes in hypothyroid neuropathy

A
  • primary axonal degeneration, characterized by axon shrinkage, disintegration of neurofilaments and neurotubules, and active axonal breakdown.
326
Q

shingles is causes by? what cells does it effect?

A
  • herpes varicella zoster infection
    o latent infection in perineuronal satellite cells of dorsal root ganglia
327
Q

symptoms of shingles

A
  • rash, pain, paresthesia on dermatomal region
  • weak muscles
  • postherpetic neuralgia
328
Q

who gets shingles

A
  • in elders and impaired cell mediated immunity
329
Q

most common area that lyme effects

A
  • facial palsy most common, then cervical or lumbar
330
Q

what is concurrent with Lyme disease

A

aseptic menhingoradiculitis

331
Q

triad of lyme disease and peripheral neuropathy

A

cranial nerve palsies, radiculitis, and aseptic meningitis

332
Q

changes in Lyme disease

A
  • perivascular inflammation and vascultic changes
333
Q

what is the most common hepatitis

A

hepatitis C

334
Q

hepatitis C causes

A

o cryoglobulin deposits in vasa nervorum and HCV-mediated vascultitis
o cryoglobulinemia  peripheral neuropathy

335
Q

hepatitis deposits what

A

cryoglobulin

336
Q

how does hepatitis C cause peopheral neruoapthy

A
  • liver effected which metabolized drugs and toxins which can accumulate and damage nerve cells
  • chronic liver disease, like in hep B and C can cause B12 and folate deficiencies (which nerves also need to function)
337
Q

leporsy is cause by

A
  • acid-fast bacteria Mycobacterium leprae
338
Q

leprosy effects

A

skin and peripheral nerves

339
Q

types of leprosy

A

: tuberculoid leprosy to lepromatous leprosy and borderline leprosy

340
Q

which type of leprosy is neuropathy most common in

A

borderline leprosy

341
Q

tuberculoid leprosy

A

o asymmetric neuropathy and confined to nerves under the skin lesion

342
Q

lepromatous leprosy

A

o slow progression but extensive; bilateral symmetrical distal polyneuropathy

343
Q

borderline leprosy

A

o most severe, rapid and multiple nerves effected

344
Q

which leprosy is most severe

A

borderline leporsy

345
Q

HIV causes what type of neuropathy

A

distal symmetric polyneuropahty
axonal degeneration in distal nerves

346
Q

HIVother tytpes of neuropathy

A
  • inflammatory demyelinating polyradiculoneuropathy
  • vasculitic neuropathy; mononeuropathy or mononeuropathy multiplex
347
Q

drugs for HIV AIDS can resemeble

A

distal symmetric polyneuropathy

348
Q

lymphocyte infiltrates in HIV and neuropathy

A
  • diffuse infiltrative lymphocytosis syndrome; axonal polyneuropathy
  • CD8+ lymphocytic infiltrates
349
Q

alcoholism causes deficiency in

A
  • Thiamine (B1), B6, B12, folic acid
350
Q

ethanol effects

A

nerve function

351
Q

alcohol and peripheral neuropathy

A
  • Impaired blood flow to extremities
  • Inflammation
  • Metabolic changes to glucose metabolism and insulin resistance
  • ROS
352
Q

Which of the following statements accurately describes the pathophysiology of peripheral neuropathy associated with vitamin B12 deficiency?
A) Vitamin B12 deficiency neuropathy is primarily caused by dietary deficiencies alone.
B) Impaired absorption, parasite infections, and dietary deficiencies are unrelated to the pathophysiology of vitamin B12 deficiency neuropathy.
C) Pernicious anemia, resulting from impaired intrinsic factor production, can contribute to vitamin B12 deficiency neuropathy.
D) Vitamin B12 deficiency neuropathy is exclusively caused by parasite infections.

A

C) Pernicious anemia, resulting from impaired intrinsic factor production, can contribute to vitamin B12 deficiency neuropathy.

353
Q

2) Which microbial infection is primarily associated with peripheral neuropathy due to direct nerve damage?
A) Shingles (Herpes zoster)
B) Lyme disease (Borreliosis)
C) Hepatitis B virus (HBV)
D) Leprosy (Hansen’s disease)
E) HIV (Human Immunodeficiency Virus)

A

D) Leprosy (Hansen’s disease)

354
Q

3) Which of the following mechanisms best explains the association between alcoholism and the pathophysiology of peripheral neuropathies?
A) Elevated levels of vitamin B12 and folate
B) Enhanced neuronal regeneration and repair
C) Impaired metabolism of thiamine and other essential nutrients
D) Increased production of nerve growth factors

A

C) Impaired metabolism of thiamine and other essential nutrients

355
Q

clock genes are

A
  • Intracellular time system, regulates 24 hour circadian rhythm
356
Q

clock genes are

A
  • Entrained by light dark cycles, exercise and eating
357
Q

zeitgebers

A
  • Entrained by light dark cycles, exercise and eating
358
Q

examples of clock genes

A

Clock, Bmal1, the “period” genes (Per1, Per2, Per3), Cry1, and Cry2

359
Q

what are clock genes synchronized by

A
  • Increase and decrease over 24 hours; synchronized via melatonin fluctuations
360
Q

clock genes ARE NOT responsible for

A

SCN intrinsic rhythms

361
Q

clock geners ARE responsible for

A

for intrinsic rhythms of rest of body (i.e muscle, brain, leukocytes) and are modified by sleep and hormones

362
Q

clock genes regulate ___% of human genome

A

25%

363
Q

clock genes are metabolic…

A

cell growth, body temp, metabolism, immune…

364
Q

what type of molecule is melatonin

A

amphipathic

365
Q

melatonin is carried by

A

albumin

366
Q

melatonin_____ by blue light

A

suppressed

367
Q

blind and melatonin

A

abnormal

368
Q

live in dim light effects melatonin

A

more sensitive to light and secrete more melatonin in response to it

369
Q

type of signling for melatonin to retina

A

paracrine signal

370
Q

melatonin increases the expression of which antioxidant enzymes

A

superoxide dismutase and glutathione peroxidase

371
Q

melatonin blocks

A
  • Blocks Bax proapoptotic activity and reduce caspase 3
372
Q

melatonin is anti inflammatory via

A

inhibit cyclooxygenase (COX) enzyme  reduce prostaglandin and leukotriene

373
Q

analgesic effect of melatonin

A

MT1 and MT2 reduce pain transmission in dorsal horn neurons

374
Q

melatonin as an antioxidant

A

(protect against cancer, reduced BP, neuroprotectant

375
Q

melatonin is found where

A
  • Localized in mitochondria in many tissues
376
Q

if melatonin fluctuates properly in a day what effect does it have of sugars and fats

A

insulin sensitive and decrease fat mass and hyperglycemia

377
Q

cardiometabolic conseuqeunces of disrupted sleep

A
  • Increase visceral fat, decrease insulin sensitivity, obese/ metabolic syndrome, dyslipidemia
378
Q

complications of obstructive sleep apnea

A
  • Premature death; respiratory events increase SNS  hypertension
  • Intrathoracic negative pressure swings  alter preload and afterload  cardiac remodeling
  • Hypoxia  vasoconstrict, increase RV afterload
  • Increase thrombosis and free radicals  atherosclerosis
  • Atrial fibrillation and atrial flutter
379
Q

sleep deprivation has what effect on mens reproductive health

A

decrease testosterone

380
Q

sleep deprivation and wehich sleep hormone have what effect on Womens health

A
  • Melatonin in ovarian follicular fluid; protect oocytes from oxidative stress
    o Low levels = infertility
381
Q

which homrones increase in sleep

A
  • TSH, GH, prolactin increases in sleep
    o GH and prolactin increase T cell proliferation and promote Th1
382
Q

which homrones decrease in sleep

A
  • Cortisol, NE and E decrease in sleep
383
Q

increased melatonin in kids helps to suppress____

A
  • Increased melatonin levels in children help to suppress GnRH secretion from the pituitary
    o Decline of melatonin production during adolescence is linked to onset of puberty
384
Q

immune and sleep

A
  • Increase Il2 and IFN gamma
  • Decrease IL10
  • TH1 adaptive immunes response at 3am
  • NK increase in late AM (blocked if sleep problem)
  • IL6 and TNF (pro inflame) increase in night
  • More Th1 than Th2 in sleep
385
Q

sleep disorders and cancer

A

increase prostate cancer

386
Q

shift workers and circadian

A

circadian genes affect genes for cell division and DNA repair

387
Q

circadian rhythm and gut microbiome

A
  • Microbes don’t express clock genes
  • Microbes may be able to regulate circadian rhythm
  • High fat diet changes clock gene (per2, ARNTL) in liver via butyrate
388
Q

seizures are

A
  • sudden, uncontrolled electrical disturbance in the brain
    o changes in behavior, movements, feelings, and levels of consciousness
389
Q

seizures are a _____ burst in large cortical region

A
  • hypersynchronized excitatory burst in large cortical region
    o individual neuron: paroxysmal depolarization shift (long lasting influx of ca2+ triggers Na+ VGC for influx and repeat APs)
    o spike discharge: summation of field APs
390
Q

spread activation to surrounding neurons in seizure by

A

o increased K+ (RMP more positive and easier to reach threshold)
o Accumulate Ca2+ in presynaptic terminals
o NMDA receptor  additional Ca2+ influx

391
Q

4 classifications of seizures

A
  1. focal seizures
  2. generalized seizures
  3. motor onset
  4. non motor
392
Q

focal seizures

A

a. from 1 brain region- structural problem
i. Intact or impaired awareness
ii. Motor or nonmotor at onset

393
Q

generalized seizures

A

from both cerebral hemisphers

394
Q

motor seizures

A

tonic-clonic

395
Q

non motor seizures

A

a. absence seizure, sensory, autonomic or emotional symptoms

396
Q

focal seizures with intact awareness

A
  • EEG in non-seizure period is normal or brief epileptiform spikes or sharp waves
  • From medial temporal lobe or inferior frontal lobs
  • i.e. motor cortex spread from fingers to hands
  • paresis after seizure
  • Sensory changes or emotional experiences (déjà vu, fear, detachment)
397
Q

focal serizures with impaired awareness

A
  • Not loss of consciousness, but cant respond to environment (i.e. convo) and poor recollection
  • Aura, automatism
  • Full recovery of consciousness in seconds or > hours
398
Q

general seizures with typical absence seizures

A

o Sudden brief (seconds) loss of consciousness without loss of postural control
o Kids
o 100x/day “day dream”

399
Q

generalized seizures with atylical absence seizures

A

o Gradual longer lapse of consciousness
o Focal and motor symptoms
o Diffuse or multifocal structural abnormalities; neurological complications

400
Q

generalize tonic-clonic seizures

A

o From metabolic problems
o Tonic phase: contract muscles, impair respiration (cyanosis), jaw clench for 10-20 seconds
o Clonic phase: muscle relax for 1 min
o Post-ictal phase: unresponsive, muscles flaccid, salivate, incontinence
o Regain consciousness mins to hours
o Headache, fatigue, muscle pain after
**most comon

401
Q

hat is the most common type of seizure

A

generalized tonic clonic seizure

402
Q

atonic seizure

A

o 1-2 secs of postural muscle loss
o Impaired consciousness, no post-ictal confusion
o i.e. head drop or body collapse

403
Q

myoclonic seizure

A

o Muscle contraction
o From metabolic, CNS degeneration, anoxic brain injury

404
Q

epileptic spasms (generalized seizure)

A

o In infants; flex or extend proximal or truncal muscles

405
Q
  • Epileptogenesis in seizures
A

transform normal brain tissue into network that’s hyperexcitable
o i.e. congenital, head trauma, stroke, infection

406
Q

epileptogenic factors

A

promote lowering of seizure threshold

407
Q

precipitating factors for seizures

A

trigger a seizure i.e. hormones, toxic, meds, photic stimulation, stress, sleep deprivation

408
Q

ages and seizures

A
  • neonate/ infant: congenital CNS abnormal, hypoxic ischemic encephalopathy, perinatal injury, inborn errors in metabolism (ie. Pyridoxine deficiency), CNS infection
  • early child: febrile seizure
  • child: idiopathic or genetic
  • adults: CNS lesion, infection, head trauma, tumor, illicit drugs,
  • older adults: cerebrovascular disease, degenerative
  • any age: metabolic (electrolyte, hypo/hyperglycemia), renal failure, hepatic failure, endocrine, medications
409
Q

sleep depirvation and epilespsy

A
  • increase cortical excitability  generalized epilepsy
  • epilepsy affects sleep quality: increase wake time after sleep onset, reduce REM, change nREM
410
Q

taenia and worm infestations

A
  • cattle or pigs – humans eat uncooked meat
  • invades muscles
  • abdominal symptoms
    o proglottids pass in stool
411
Q

cysticerosis

A

is infection of muscle by larval cysts of taenia solium (pork tape worm)
o penetrates intestinal wall and disseminate (muscle and brain

412
Q

neurocysticerosis

A

brain infection causing adult seizure in low income countries
o CNS parasite
o Minimal symptoms then seizures and increased intracranial pressure (or death)
o MMP-polymorphism
 Increase BBB permeability

413
Q

trypanosoma brucie is from

A

parasite from bite of tse-tse fly (s.s. Africa)

414
Q

Trypanosoma brucei and sleeping sickness

A
  • Sleeping sickness; 3 years, fatal
  • Early: Fevers, headache, pruritic, lymph, hepatosplenomegaly
  • Later phase: invade CNS- disturb sleep and neuropsychiatric disorders
    o Median eminence and hypothalamus
415
Q

changes in sleep from Trypanosoma brucei and sleeping sickness

A

o No change in total sleep time (increase daytime sleep and insomnia at night)
o Similar to narcolepsy
 SOREM episodes; sudden wake to sleep
 Excess daytime sleepiness
 Sleep fragmented

BMS200 (43 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions