week 9 Flashcards
hypertension and SNS
reset baroreceptors
ADH (water retention)
vasoconstrict
increase renin and angiotensin 2
hypertensive urgency vs emergency
urgency-increase BP and treat urgent
emergency- sign of end organ damage from high BP i.e. vision, headache, polyuria
vasculitis
▪ Large arteries
* temporal arteritis,
▪ Small and medium-sized arteries
* Polyarteritis nodosa
* Thromboangiitis obliterans
▪ Small and medium-sized arteries and veins
* Granulomatosis with polyangiitis,
vasculitis
inflam and die blood vessel
granulomas
Th1/Th17
type 3 hypersensitivity
Anti-neutrophil cytoplasmic antibodies (ANCAs) in vasculitis
p_ANCA - nucleus, bind myeloperoxidase
c-ANCA - cytoplasm, bind proteinase 3
end up recruiting leukocytes
raynauds
bilateral ischemia to finger and toe from vasospasm
worse in cold or stress
SA node in
right atrium, close to the entrance of the superior vena cava
ecg for
ECG leads only “notice” changes in membrane potential
normal sinus rhythm
regular or regularly irregular
p wave followed by QRS
QRS has P before it
constant PR
QRS < 100ms
if PR interval is prolonged then
AV node dysfunction
what varies with heart rate and how to adjust
QT (ventricle depolarize) so do QT corrected= qt? squareroot R-R
ST problems
elevation or depression
should be a flat line
dysrythmias
re-entry - normal depolarization wave enters pathological space in the heart
ectopic foci/ abnormal automaticity: make automatic in previously non pacemaker cells
triggered activity- abnormal depolarization of ventricles before original AP completed
atrial fibrilation
ectopic foci
no p wave, irregular irregular
atria flutter
re entry from fibrosis
AV blocks
1st degree: prolong PR
2nd:
I: prolong PR until QRS is dropped
II: consistent PR with sudden QRS drops
3rd: no impulse reaches ventricles from atria; inpendent rates
alpha block or alerting response
when focus on something switch from alpha to beta
alpha=
eye closed and mind wanders
beta=
open eye and wide awake
stages of sleep
N1 (transition from wake to sleep)- theta, slow eye move
N2- k complex, sleep spindle, no eye move
N3 and 4- delta, deep sleep, no eye move
REM- rapid eye, no MSK movement
limb movements in which sleep
n1-3
why no movement in rem
GABA inhibit spine
arousala system
- arousal system in mid brain and pons
- Locus ceruleus - norepinephrine
- Raphe nucleus - serotonin
- Tuberomamillary body-
histamine - Acetylcholine has multiple nuclei in the brainstem that are important in arousal
- Periaqueductal gray - dopamine
ventrolateral pre-optic nucleus (VLPO) in the hypothalamus for
sleep
release GABA and galanin
stabilizing nuclei in hypothalamus for
▪ Orexin – projects to both the arousal systems and to the VLPO
–> inhibit VLPO = awake
▪ Melanin-concentrating hormone (MCH) – also projects to arousal system
–> in REM sleep inhibit the monaminergic arousal system = sleep
rem on vs off neruons
rem off stimulate by NE and serotonin and orexin
melatonin made in
pineal gland
melatonin made from what amino acid and enzyme needed
tryptophan –> serotonin then via AANAT –> melatonin
narcolepsy
daytime sleep
lose orexigenic neruson
cataplexy
muscle weakness without loss of consciousness
restless leg
iron deficiency
basal ganglia and SN
OSA
5 or more episodes of obstructive apnea
or hypopnea during one hour of sleep
- Apnea = cessation of airflow for ≥ 10 seconds during sleep, despite respiratory effort
- Hypopnea=a≥30%reductioninairflowforatleast10 seconds during sleep that is accompanied oxygen desaturation or waking
rem sleep behaviour
act out dreams i.e. kick and punch
should have neurons in rem that stop movement
