FUCK PART 2 Flashcards
alcoholism and peripheral neuropathy
-which nutrients
-nutrient not absorbed: B12, B6, B1 (thiamine), folic acid
toxic ethanol
impaired blood flow
inflammation
ROS
metabolic- glucose and insulin resistance
EEG in sleep measure
dont measure AP directly; instead measure different in potential and cell body
waves from high frequency to low frequency (and kind of lower amplitude to higher amplitude)
BATD
beta= 13-30Hz
alpha= 8-18Hz
theta= 4-8Hz
delta= 0.5-4Hz
beta
eyes open, awake, concentrate
alpha
eyes closed, relaxed
theta
light sleep
delta
deep sleep
alpha block/ alerting response
alpha –> beta when focus
which sleep stages have large axial movements and which have no movement
move= NREM
no move= REM
eye movements in sleep stages
N1= eye slow roll
rest of NREM= no eye move
REM= rapid
N1
transition from sleep to wake
theta
slow and rolling eye movement
N2
light sleep
K complexes and sleep spindles
no eye movement
N3
deep sleep
delta
thalamus and cortex
minimal eye movement
less if old
kids sleep
50/50 REM and N3
REM
rapid eye movement
no MSK movement (bc GABA)
recall dreams
last sleep stages
theta but NOT synchronized
sleep architecture
1st period is longest, rest are 90-120 mins
arousal system
locus coreulus- NE
raphe nucleus- serotonin
tubermamillary body- histmaine
Ach- many brainstem nuclei
dopamine- periaqueductal gray
ventrolateral pre optic nucleus (VLPO) release which neurons
GABA and galanin
2 REM states from VLPO
REM on= lateral pontine
REM off= pons
stabilizing nuclei (lateral hypothalamus) in sleep
orexin: activate arousal, inhibit VLPO
melanin concentrating hormone (MCH): inhibit arousal
2 drivers of sleep
- circadian rhythm
- homeostatic signal: adenosine build up
-caffeine is A2a antagonist
REMon vs REMoff stimuli
REMon stimulated by cholinergic input
REMoff stimulated by NE, serotonin, orexin
melatonin is made where? metabolite of?
made in pineal gland
metabolite of serotonin
dark and light effects an melatonin
dark: PVN activates SNS –> release NE and activate pineal gland –> melatonin –> SCN
light: SCN inhibits PVN
steps to make melatonin
tryptophan –> serotonin 5 HTP [[AANAT]] –> N-acetylserotonin [[HIOMT]] –> melatonin
NE (catecholamines) act on beta 1 receptor to make AANAT
entrain SCN
retinohypothalamic fibers relay light
MT2 melatonin receptors
MT melatonin receptors
MT1 decreases sleep latency
MT2 increases sleep time
narcolepsy
excessive daytime sleepiness
what sleep stage does narcolepsy effect
REM intrusion: cataplexy (weak muscle), sleep paralysis, hallucination
type 1 narcolepsy
narcolepsy + cataplexy
cause of narcolepsy + cataplexy
loss of orexinergic neurons (autoimmune, molecular mimicry via strep or infection)
hypnagogic vs hypnopompic hallucinations in narcolepsy? more common?
hypnagogic; while going to sleep
hypnapompic; while awaken (more common)
what happens in sleep stage or narcolepsy
enter REM quickly
treat narcolepsy
antidepressants to increase NE and serotonin and stimulate REMoff
since loss orexinergic neurons and enter REM quickly
restless leg syndrome and periodic limb movement disorder
RLS: when awake? need to move legs, triggered by rest, inactivity, sleep
PLMD: occurs during sleep, kick legs
RLS and PLMD are? effect which brain area
movement disorders- basal ganglia and substantial nigra
causes of RLS and PLMD
iron deficient
increased/ abnormal dopamine
treat RLS and PLMD
with dopamine agonist (even though increase DA in day its decreased at night)
Obstructive sleep apnea
> 5 OA or hypopnea episode in 1 hour
> 15= severe
apnea vs hypoapnea
apnea= no air for >10 secs
hypoapnea= >30% reduction in airflow for 10 secs
what sleep stage is OSA worse in
REM
causes of OSA
pharyngeal collapse from negative pressure
obesity, male
co2 sensitivity
septal deviation or nasal polyps
diagnose OSA
polysomnogram
parasomnia
abnormal behaviour that Arise from or during sleep
types of parasomnias
sleep walking
sleep terrors
REM sleep behaviour disorder
who and what sleep stage does sleep walking and sleep terrors happen in
N3, kids
sleep walking and sleep terrors
SW: N3, early evening
ST: scream, N3, tachycardia, hyperventilate
REM sleep behaviour disorder (parasomnia)
act out dreams; kick, punch
who does REM sleep behaviour disorder happen in
older
REM sleep behaviour disorder from
neurodegeneration of interneurons that cause paralysis in REM
HIV and peripheral neuropathy
-distal symmetric
-inflammatory demyelinating polyradiculoneuropathy
-AIDS drugs can cause toxic neuropathies
-CD8+
chemotherapy induced peripheral neuropathy
glove and stoking
platinum [ ] in tissue
shingles cause
herpes varicella zoster
shingles and peripheral neuropathy
latent; post herpetic neuralgia
dermatomes
infect perineurial satellite cells
triad of Lyme disease and peripheral neuropathy
cranial nerve palsy
radiculitis
aseptic meningitis
what are causes of acute pericarditis
viral-coxackie A and B, echovirus and idiopathic most common
strep, staph, TB, RA, SLE
what makes pain in acute pericarditis better
sitting up and leaning forward
acute pericariditis
common, fibrinous inflammation
pericardial friction rub
increased ECF= pericardial effusion
diagnose acute pericariditis
echocardiography
prognosis of acute pericaridits
self resolve or NSAID, aspirin
complication of acute pericarditis
cardiac tamponade, progress to constrictive pericarditis
constrictive pericarditis
pericardium scars after acute pericarditis
restrict cardiac filling
decrease end diastolic volume, venous congestion, fatigue, neck vein distended, hepatosplenomegaly
pericardial tamponade (complication of acute pericarditis)
accumulate fluid, obstruct flow to ventricles
can cause obstructive shock
myocarditis can lead to
dilated cardiomyopathy, conduction blocks
causes of myocarditis
echovirus, coxsackie, Lyme, tryponosmitatis cruzi, SARS CoV2, rickets
pathophysiology in myocarditis
adaptive immune response: form granuloma, release cytokines, alter ECM, fibrosis and dialtion
mehcanism in bacterial endocarditis
vegetation + thrombus
what part of the heart does bacterial endocarditis involve
valve
pathophysiology in bacterial endocarditis
form thrombus –> bacteria colonize it –> break off and cause stroke or obstruction
vegetation: mass of platelets, fibrin etc. –>break off and spread
causes of bacterial endocarditis
from bacteria: dental/ gingival
bad, acute: strep, staph, enterococcus
less bad, slow: HACEK
symptoms of bacterial endocarditis
fever, anorexia, heart murmur, splenomegaly, myalgia…
infective endocarditis key findings
osler nodes, janeway lesions, roth spots
Lyme disease is caused by
barrelia burgdoferi
Lyme disease need
a réservoir animals
baby ticks (nymphs) better at transmitting disease
Lyme disease binds what proteins in the body
complement regulatory proteins
2 stages of Lyme disease
stage 1: erythema migrans rash
stage 2: effect many organs via blood vessels –> myocarditis, CNS, joints, arthritis
Lyme disease can cause inflammation in what
myocarditis
diagnose lyme
2 tiered serological testing and EISA immunoblot test
antibodies so dont know if past or current infection
endocarditis microbes virulence factors - strep
strep have dextrans to adhere to thrombotic vegetation or valve damage
-bind platelet fibrin complexes
-fimA
fibronectin is usually hidden by endothelium, but exposed by strep
virulence factors in strep (bacterial endocarditis)
dextrans and fimA and mucopolysaccharide biofilms
also exposes fibronectin
endocarditis microbes virulence factors - s aureus
produce tissue factor to build clots, invade vegetations
endocarditis microbes virulence factors - HACEK
in oral cavity to blood stream via floss or dental work
what entrains clock genes
zeitgebers: light/dark, food, exercise
clock genes synchronized to 24 hours via
-synchronized to 24 hours via melatonin
clock genes for the intrinsic rhythm of
the rest of the body NOT the SCN
melatonin is carried by
albumin
melatonin paracine signal to the
retina
melatonin increases antioxidant enzyme
superoxide dismutase and glutathione peroxidase
what does melatonin block
block Bax proapoptotic and caps 3
inhibit COX and prostaglanding= anti-inflammatory
melatonin as analgesic
decrease pain via MT1 and MT2
melatonin is localized in the
mitochondria
sleep deprivation and mens and Womens health
decrease testosterone
follicular fluid- ROS and infertile (melatonin is protective)
what hormones increase and decrease in sleep
increase: TSH, GH, prolactin
decrease: cortisol, NE, E
melatonin suppressed GnRH (puberty?)
melatonin and immune response
Th1 response
NK
diet and sleep
high fat diet changes clock genes
hypothyroid and peripheral neuropathy
distal or proximal?
axonal degeneration or myelin desegmentation?
proximal myopathy and carpal tunnel
primary axonal degeneration
how does hypothyroid cause peripheral neuropathy
weight gain and water retention, mucopolysaccharides, hyaluronic acid
energy deficit from nutrient oxidation: decease ATP, accumulate glycogen, decrease Na+/K+ pump
Hepatitis B or C more common in peripheral neuropathy
Hepatitis C
what does hepatitis C have for peripheral neuropathy
cyroglubulimenia (a protein leading to vasculitis)
mechanisms of hepatitis B and C (autoimmune) and peripheral neuropathy
-directly invade liver and nerves
-liver metabolizes drugs and toxins
-B12 and folate deficiency from chronic liver disease
leprosy is caused by
mycobacterium leprae
leprosy affects peripheral neuropathy via
direct nerve damage
3 types of leprosy
-tuberculoid leprosy
-lepromatous leprosy
-borderline leprosy
tuberculoid leprosy and peripheral neuropathy
asymmetric, around skin lesion
lepromatous leprosy and peripheral neuropathy
extensive bilateral symmetric distal
borderline leprosy and peripheral neuropathy
severe
most common leprosy that causes peripheral neuropathy
borderline leprosy
seizures are
an electrical disturbance
types of serizures
focal seizure
generalized seizures (tonic clonic, absence etc)
focal seizures
1 region of brain effected
EEG shows epileptiform spikes (medial temporal or inferior frontal lobe)
types of focal seizures (1 region of brain)
-intact or impaired awareness (impaired= cant respond to environment, automatic behaviour)
-motor or non motor
generalized seizures impact
both hemispheres of the brain
typical absence seizures vs atypical absence seizure
typical = brief loss of consciousness but not posture, common in kids, looks like “blanking out”
atypical= longer loss of consciousness
tonic-clonic seizures cause
metabolic
common type of seizure
tonic-clonic seizure
tonic-clonic seizure
contract for 10 seconds then relax for 1 minute
post-ictal phase: unresponsive, flaccid, incontinence
atonic seizures vs mycolonic seizure
atonic; lose muscles for 1 second
mycologic; brief muscle contraction
epileptic spasm (seizure)
in infants, flex or extend trunk and proximal
epileptogenesis
epileptogenic factors
precipitating factors
epileptogenesis: make brain tissue hyperexcitable
epileptogenic factors: lower seizure threshold
precipitating factors: trigger seizure
spread activations in seizures (hyper excitable)
increase K+, RMP higher
accumulate Ca2+
activated NMDA receptor, increase Ca2+
epilepsy effects sleep
decrease REM, change NREM
taenia is a
tapeworm
tania tapeworm from
raw meat; pass in stool
taenia tapeworm invades
invades the intestinal wall and muscles and brain
2 types of invasions by Tania tapeworm
cysticerosis
neurocysticerosis
cysticerosis
neurocysticerosis
from taenia tapeword
cysticerosis- muscle infected
neurocysticerosis- brain infected, common in low income countries
neurocysticerosis from taenia tapeworm impacts the brain
what is the polymorphism
causes
MMP polymorphism increase BBB permeability
major cause of seizures
what causes sleeping sickness
trypanosoma bruceli (tse tse fly)
trypanosoma bruceli (tse tse fly) and sleeping sickness
common in
lasts how long
symptoms
diagnose
impact on sleep
S.S Africa
last 3 years, fatal
fever, headaches
invade CNS, disturb sleep and cause neuropsyhiatric disorders
diagnose: CSF
no change in sleep time: increase daytime sleep, and nighttime insomnia (like narcolepsy)
what is around a single nerve fiber
endoneurium
vitamin B12 deficiency neuropathy
antibodies target what?
GI symptoms
pernicious anemia- cobalamin defieicny
antibodies target parietal cells and decrease intrinsic factor
atrophic gastris and achlorhydria
B12 defiant and what thing
decrease intrinsic factor
B12 is need for what 2 cycles
1 carbon cycle: b12 as coenzyme for homocysteine –> methionine for RNA and DNA
myelin synthesis: methylmalonyl coA –> succinyl coA
what can cause b12 deficiency
nitrous oxide
which fibers are effected in b12 deficient neuropathy
large fibers
small fibers are OK
signs in B12 deficient neuropathy
bad gait, hyperreflexia, absent achilles reflex
hand goes numb 1st
2 types of degeneration that cause peripheral neuropathy
axonal degernation and segmental demyelination
% of peripheral neuropathy caused by axonal degeneration vs segmental demyelination
90% axonal
10% demyelination
2 types of axonal degenration
distal axonal degeneration
neuronopathy
what is the mechanism in distal axonal degeneration
wallerian degeneration; degeneration after area of compression/ injury
distal axonal degeneration
distal part, neruon cell body and proximal axon are spared
wallerian degeneration
neuronopathy (a type of axonal degeneration)
degeration of neuron cell body and axon (i.e. autoimmune)
segmental demyelination
myelin sheath detonates, underlying axon is ok
hereditary or immune
macrophages remove the debris
recovery and remyeliantion via Schwann cells but decreased internodal length
types of segmental demyeliantion
primary demyelination: injure Schwann cells or myelin sheath
secondary demyelination: underlying axon abnormality
hypertrophic neuropathy (from segmental demyelination)
repeated demyelination and remyelination = accumulate supernumerary Schwann cells= onion bulb
large vs small sensory fibers
large= proprioception and vibration
small= pain and temperature
peripheral neuropathy causes
metabolic: DIABETES, thyroid
B12 defieint
systemic: HIV, Lyme, hepatitis, leprosy
toxic, alcohol, chemotherapy
types of peripheral neuropathy
polyneuropathy= symmetrical
radiculopathy/polyradiculopathy= asymmetrical
mononeuropathy= 1 nerve
multiple mononeuropathies (mononeuropathy multiplex)
plexopathy= brachial or lumbosacral plexus; 1 limb
neuronopathy= nerve cell body, ganglion cells, proximal and distal
diabetic neuropathy what type of neuropathy
usually distal symmetric stocking and glove but could be many
pathway in diabetic neuropathy
polyol pathway
poll pathway and diabetic neuropathy
high blood sugar >7mmol activates the poly pathway
glucose into sorbitol via aldose reductase and NADPH
immune and vascular problems in diabetic neuropathy
immune: antiphospholipid antibodies
vascular: decrease NO, decrease Na+/K+ ATPase, decrease free carnitine and myoinostiol, increase homocystinemia
anti-arrhythmic medications
- prevent Na+ influx
- beta blockers
- block K+; prolong refractory
- block Ca2+
cardiac ischemia findings on ECG
inverted T wave
ST elevation
3 types of conduction block
1 2 and 3 degree
1st degree AV conduction block
prolonged PR, asymptomatic, increased vagal tone of fibrous
two types of 2nd degree AV conduction block
type 1 (wenckebach): progressive prolong of PR until QRS is dropped
type II: consistent PR, QRS suddenly drops, more serious –> progress to 2rd degree and cardiac arrest
3rd degree AV conduction block
no impulse from atria reach ventricles
bradycardia, heart failure, syncope, decrease CO
regular P and QRS, but not coordinated, slow HR
ECG findings in all conduction blocks
1st degree= prolong PR
2nd degree type I= progressively prolong PR until QRS dropped
2nd degree type II= consistent PR, QRS suddenly drops
3rd degree= regular P and QRS but not coordinated
% of primary vs secondary hypertension
90% primary
10% secondary
mechanism in primary hypertension
increased tone and resistance in arterioles, release less NO, arteroscleosis (deposit ECM, hypertrophy)
vascular changes in kidney (regulate BP)
increase SNS: alpha 1 vasoconstriction, increase ADH, increase renin and AT 2
increase WBCs to kidneys
increase Na+ –> Th17 and ILC3
insulin resistance and obesity
what are the systems most frequently impacted in secondary hypertension
kidneys and SNS
also OSA, medication, endocrine…
hyperthryoid= increase SBP
hypothyroid= increase DBP
diagnosis of hypertesnion
> 180/110 = immediate diagnosis
automated: >135/ 85 or >130/80 if diabetic
in office: >140/90
hypertensive urgency
systolic >180 or diastolic >120
hypertensive emergency
end organ damage
malignant hypertension
> 180/120, end organ damage, fibrinoid necrosis
antihypertensive medications
-Ca2+ channel blockers
ACE inhibitors: decrease angiotensin and vasoconstriction and stop ACE from desrtroying bradykinin (so bradykinin can increase and increase NO to vasodilate)
AT2 receptor (ARB) blockers
alpha receptor blockers: decrease NE and E
type of reaction in vasculitis? immune?
inflammation and necrosis
Th1/ Th17
type III hypersensitivity reaction: immune complex
secondary vasculitis
hepatitis, autoimmune, medications
types of vasculitis
temporal arteritis
polyarteritis nodosa
thromboangitis obliterans
granulomatous with polyangitis
most common type of vasculitis, especially in elders
temporal arteritis
temporal arteritis affects
large arteries
pathology in temporal arteritis? arteries effects? symptoms?
patchy granulomatous, caroitd artery branches: temporal and ophthalmic
temporal headache, vision loss, poly myalgia rheumatica
diagnosis and treatment of temporal arteritis
diagnose: ESR/CRP, ultrasound of temporal artery
treat: glucocorticoids
polyarteritis nodosa cause
hepatitis B
polyarteritis nodosa effects
medium and small arteries
ogans in polyarteritis nodosa
many organs, but rarely lungs
kidney (increase BP)
MSK (arthritis, myalgia)
peripheral neuropathies (mono multiplex)
skin findings in polyarteritis nodosa
raynauds
pupura and nodules
raynauds in which vasculitis
polyarteritis nodosa
Thromboangitis obliterans effects the
medium and small arteries
who is thromboangitis obliterans most common in
men, smokers
thromboangitis obliterans presentation
distal arm and leg –> occlusion and ischemia –> ulcers and claudication
vessels impacted by granulomatous with polyangitis
small and medium arteries and veins
granulomatous with polyangitis symptoms
URTI, LRT, kidney: sinus, dyspnea, renal failure
flaring disease
diagnose granulomatous with polyangitis
cANCA
what are ANCAs
anti-neutrophil cytoplasmic antibodies
increase cell surface expression in inflammation
p-ANCA and c-ANCA
p-ANCA: nucleus, bind myeloperoxidase
c-ANCA: cytoplasm, bind proteinase 3
Raynauds presentation
bilateral, asymmetric ischemia of fingers and toes
rarely ulcers or gangrene
raynauds cause
transient vasopasm
raynauds worse with
cold and stress
raynauds and autoimmune
lupus
3 phases of raynauds
- vasoconstrict (white)
- cyanosis (blue)
- hyperemia (red) - blood flow restored
SA node location
right atrium, near vena cava
heart rate is found on ECG by
R-R interval
300/ # of boxes
rhythms on ECG
regular
regularly irregular
irregularly irregular (atrial fibrilation)
normal sinus rhythm criteria
SA as pacemaker
regular or regularly irregular
each P wave followed by QRS
each QRS has a P wave before
constant PR interval
QRS <100ms (2.5 boxes)
long PR interval=
AV node dysfunction
QT varies with
heart rate
QT corrected
QTc = QT/ (square root of R-R)
abnormal Q wave
MI
ST segment pathology
elevated: STEMI, hyperkalemia, RBBB
depressed: NSTEMI, hypokalemia, LBBB
T wave problems
tall: hyperkalemia
small: hypokalamie
inverted: MI, ventricular hypertrophy
P wave problems
-different pacemaker if it changes beat to beat
-absent= atrial fibrillation
-more P waves than QRS= heart block
3 causes of dysrhythmias
- re-entry
- ectopic foci or abnormal automaticity
- triggered activity
re-entry
normal depolarization enters ischemia area and cant contract –> slower conduction
if complete refractory then depolarize= tacchycardia
area of fast and slow conductance
ectopic foci or abnormal automaticity
increase Ca2+ decrease K+
scar tissue changes electrolytes (inhibit Na+/K+ - accumulate Na+/Ca2+)
make non-pacemaker cells automatic= ectopic foci
IR K+ = decrease refractory period
triggered activity
normal AP then abnormal ventricular depolarization before AP complete
i.e. premature ventricular contractions
most common type of dysrhythmia
atrial fibrillation
atrial fibrillation has ___ p wave
no
what dysrhythmia is the leading cause of stroke
atrial fibrillation
atrial fibrillation findings
ectopic foci, re-entry
irregular irregular HR
atrial flutter
re-entry bc of fibrosis
atrial rate 300bpm
sinus tachycardia
increase HR and CO
from exercise, stress, excess catecholamine OK, bad if at rest
paroxysmal supraventricular tachycardia
at atria or AV node
re-entry
premature ventricular contraction- what is it initiated by
heartbeat from the purkinje fibers
premature ventricular contraction on an ECG
wide QRS; single, double, triple
premature ventricular contraction - what dysrhythmia
ectopic nodal automaticity, triggered activity, re-entry
idioventricular rhythm - what on an ECG
no p wave, prolonged QRS
idioventricular rhythm- what happens
SA node isn’t working, ventricles take over
HR in idioventricular rhythm
slow regular, <50bpm
ventricular tachycardia cause
ischemic heart disease
life threatening
ventricular tachycardia HR
100-250bpm, > 3 ventricular beats
ECG for ventricular tachycardia
wide QRS
dysrhythmias in ventricular tachycardia
re-entry, triggered activity, enhanced automaticity
CO and SV in ventricular tachycardia
decreased
ventricular tachycardia can lead to
ventricular fibriliation
HR and CO in ventricular fibrillation
irregular, >300bpm, decreased CO
what can ventricular fibrillation lead to
sudden cardiac death in minutes
dysrhythmias in ventricular fibrillation
purkinje automaticity, re-entry , triggered activity
ECG in ventricular fibrillation
no P wave, QRS or T wave
trosades de points is a type of
ventricular tachycardia
ECG on torsades de pointes
twisting ECG, varied QRS
prolonged QTc (prolonged repolarization)
torsades de pointes can progress to
ventricular fibrillation; cardiac death
