CMS final key notes Flashcards
whats predominant in first half of sleep vs second half
1st- N3
2nd- REM
who’s more likely to get insomnia
women
insomnia definition
A repeated difficulty with sleep initiation, duration, consolidation, or quality that occurs despite adequate time and opportunity for sleep and results in some form of daytime impairment
distress and impair daytime functioning
chronic vs short term vs other insomnia disrosder
chronic- 3x/week for 3 months
short term- 1 to 3 months
what distinguished short term from chronic insomnia
identifiable cause (i.e. stressful life event, medications, withdrawal from drugs)
genes and molecules in chronic insomnia
ApoE4, orexin, histamine, gaba, serotonin, melatonin
Zeitgebers examples
social activities, meals, light-dark cycle
biological clock in
SCN of hypothalamus
ganglion cells of retina send information to SCN
SCN stimulate pineal gland to release melatonin
when does melatonin peak
3 hours before waking
normal circadian intrinsic rhythm
> 24 hours- get to 24 hours by zeitgebers
intrinsic vs extrinsic circadian rhythm sleep disorder
extrinsic: shift work, jet lag
intrinsic: advance sleep phase disorder, delayed sleep phase disorder etc
Delayed Sleep-Wake Phase Disorder
Delayed sleep and wake times relative to what is desired or expected à inadequate sleep and resultant daytime functional impairment
lose at least 2 hours of sleep
sleep inertia (confused when wake up)
depression, excess caffeine and light
treat: sleep hygiene
Advanced Sleep-Wake Phase Disorder
Excessive evening sleepiness and early morning awakening
i.e. if out late with friends will still wake up early
hypothesis: internal circadian clock <24 hours
treat: evening bright light therapy
Irregular Sleep-Wake Rhythm Disorder
Failure of the circadian rhythm system to consolidate sleepàmultiple short periods of sleep and wakefulness
> 3 periods of wakefulness for at least 1 hour during 24 hrs
esp in dementia
from lack of external cues (zeitgebers)
treat: behavioural and melatonin
jet lag disorder
> 2 time zones (can only adjust to 1-1.5 time zones per day)
eastward travel worse
shift work disorder
insomnia occurs despite sleep debt
rotating schedules bad (better if swings progress later in day instead of earlier)
try to get 3-4 hours of “anchor” sleep at same time every day
non-24 sleep-wake rhythm disorders
Results from a circadian rhythm system not entrained or running without
apparent regulation
i.e. blindness
treat: Rx Tasimelteon (melatonin-receptor agonist)
narcolepsy
excessive daytime sleepy with 15 minute sleep attacks
cataplexy (muscle weak)
sleep paralysis (muscle flacid + conscious)
hypnogogic or hypnopompic hallucinations
narcolepsy and REM
abrupt transition into REM
narcolepsy after nap
feel refresh
narcolepsy type 1 and type 2
type 1- low levels of orexin or episode of cataplexy
type 2- normal orexin and no episodes of cataplexy
idiopathic hypersomnia
-daytime sleep
-no cataplexy
etccc
klein levin syndrome
mostly young men
3-4 times a year for 2 days of hypersonic attack (i.e. 15 hour sleep)
hyrerphagia (hungry), hypersexial
hypersomnia from
medical condition (i.e. parkinsons, POTS)
medication/substance
infufficient sleep
psychiatric disorder
paraomnia is
abnormal behaviour during sleep
types of parasomnias
non-rem: sleep walking, sleep terrors
REM: nightmare, sleep paralysis
other: exploding head, eating disorder, enuresis
sleep terrors
N3
sleep walking
amnesia of the walking event
N3 or in REM
nightmares
during REM
enuresis
most in kids
period limb movement disorder
during sleep
usually has hypoapnea
Restless legs syndrome
can be while awake
-worse with rest, relieved by movements, occurs in evenings
conditions tha mimic sleep loss DDX
30-40% = mental health disorder
anxiety, depression, GERD, COPD, brain tumor, medications, shift works, OSA
alcohol use disorder effect sleep
acute: decrease latency and reduce REM and increase N3
Chronic: increase N1, decrease REM
caffeine cocaine and stimulates effect
NREM and sleep latency
OSA morbidity
HTN, heart fail, diabetes
OSA
collapse of upper airway –> hypoapnea or apnea
mild: events 5-15 per hour
moderate: 15-30
severe: >30
OSA: >5 with daytime sleepiness
apnea vs hypoapnea
cant breath 10 secs
30% reduction
highest LR for sleep apnea
nocturnal chocking/ gasping
morning headache
combination of symptoms is better…. alone not very heppful
esp snorning is not helpful to diagnose, good LR- though
good questionnaire for sleep apnea
STOP bang score of 3
neck circumference
good for OSA increased risk
- Insomnia: complaints of difficulty initiating sleep or staying asleep
- Hypersomnia: difficulty staying awake during the day
- Parasomnia: abnormal movements or behavior during sleep
- Circadian rhythm disorders: timing of the sleep–wake cycle at undesired or inappropriate times over a 24-hour day
x
gold standard of sleep questionaires
Pittsburg sleep quality inventory PSQI
godl standard test for OSA
polysomnography
sleep diary
Identifying behaviours or patterns that may be targeted for intervention
1 cause of death
ischemia heart disease
75% of myocardial infarction from
plaque rupture (atherosclerosis)
risk factors for atheroscleorsis
male (decrease estrogen), hypertesnion, smoking , DM, chylamida, lp(a)
atherosclerosis symptoms depend on artery effected
I.e. coronary heart disease: angina/ chest pain
PAD: leg cramp
vertebral artery disease. weak body on one side
mesenteric: weight loss, diarhea
general: stroke, fatigue, dizzy, low back and chest pain, ED, cold and pain hand and feet
skin in atheroscleorsi
xqnthoma
atherosclerosis labs
LDL, glucose, hsCRP
look for atherosclerotic lesion
angiography
complications of atherosclerosis
- occlude vessel
- disrupt plaque (hemorrhage or rupture)
- emboli
- aneyrsym
- peripheral vascular disease (claudication)
peripheral vascular disease
outside heart and brain
peripheral artery disease
in major arteries distal to the aortic arch
upper and lower extremities
classic/ intermittent claudication
fatigue, muscle discomfit, cramp, pain in lower limbs
induced by exercise and relive by rest in 10 mins
in 10-30% of patients with PAD
LR+ 3.30
Edinburgh claudication questionnaire LR+11
skin in PAD
ulcers, gangrene, pallor them rubor, cold skin, dystrophic nails, distal hair loss, diminished pulses, bruits
best LR+ for PAD
8.1
abnormal posterior tibial pulse
44.6 LR+ if DP and PT pulses absent
ankle brachial index (ABI) for PVD/PAD
for lower extremity hemodynamics
screening fo PAD
USPSTF- insufficient evidence for routine screening if asymptomatic
AHA/ACC says people with increased risk should be assessed
ABI screening for PAD
ABI if have history or exam findings of PAD
if have increased risk of PAD but no findings then can also do
ABI screen if diabetic > 50 yrs old
critical limb ischemia
in 1-2% of PAD/PVD cases
ischemia of collateral vessel that maintain limb perfusion
sx: >2 week (chronic) ischemic rest pain, ischemic wounds, tissue loss, gangreene
nocturnal symptoms, worse at night
acute limb ischemia
abrupt interruption of arterial blood flow to an extremity
i.e. cold, pain, pale, diminished pulses, sensory or motor
labs for PVD
CBC, electrolytes, fasting glucose, lipids, kidney function (creatinine, urinalysis)
althrought CRP, lp(A), and homocysteine are all risks for PVD–> dont help with clinical benefit
duplex ultrasonography/ doppler
determine PAD location
MRA or CTA (angiography)
for vascular imaging
gold standard for PAD diagnosis
catheter-based angiography
DVT
unilateral
neurogenic claudication (spinal stenosis)
narrowing of foramen, esp lumbar
degenerative osteoarthritis or spondylosis
low back and leg pain, worse with standing or walking (i.e. exercise) and better when lying or sitting
better with flexion, worse with extension
venous thromboembolism (VTE)
blood clotting conditions
includes deep vein thrombosis DVT and pulmonary embolism PE
PE more fatal
DVT: in legs (swell, warm, red, pain)
PE: clot travels to and blocks lungs (SOB, chest pain, rapid HR)
virchow triad VTE
hypercoagulability
vascular damage
circulatory stasis
PE develops in 50% of patients with proximal lower DVT
low oxygen (hypoexmai)
dyspnea**, tachypnea, chest pain
Pulmonary embolism; wells score clinical prediction rule
signs of DVT, alternative diagnosis less likely, HR>100,…
DVT; wells score
cancer, bedridden, swollen leg, edema…
most common DVT
lower extremity 10x more common than upper extrimitiy
tests for DVT and PE
d -dimer (fibrin degradation product) if low likelihood and imaging if high likelihood
abdominal aortic aneurysm AAA
increase vessel diameter by> 50%
infalmmed and degeneration of arterial wall lead to dilation and rupture
seen in PAD
risk factors for PAD
renal dysfunction +12
heart failure +7
>65 yrs old +5
….
dysuria
pain or burn after urine
UTI
bacterial infection from uretha to renal pelvis
UTI upper vs lower
upper: kidney and ureter
lower: bladder, urethra, prostate (male)
upper less common but more severe
lower UTI
cystitis
urethritis
prostatiits
upper; pyelnoneprhitis
uncomplicated vs complicated UTI
uncomplicated: normal urinary tract
complicated: male, pregnanct, abnormal urinary tract, diabeters…
UTI most common in
young women sexually active
most common UTI
acute cytistis
acute cystitis
bladder infection
diagnose with pyuria (WBC in urine) and bacteriuria
bacteria causing acute cystitis
KEEPS
75-95% e. coli
symptoms in acute cysitis
dysuria, suprapubic pain
hematuria (blood, urinary frequency and urgency
absence of discharge, CVA tender, N/V, fever
atypical presentation of acute cystitis in older
delirium, lethargy, functional decline
high LR for UTI
self diagnosis in patients with recurrent UTI LR+4
1 symptom isn’t that helpful
combine: dysuria and frequency without vaginal discharge = LR+ of 24.6
90% likelihood of cystitis so can treat without testing
A woman with dysuria and frequency but without vaginal discharge or irritation has a 90% likelihood of having cystitis,
treat without testing
urine dipstick urinalysis
leukocyte esterase, nitrites (from bacteria), WBC, hematuria, ph, ketones, bilirubin, glucsoe
high LR+ for urinalysis for cystitis
leukocyte esterase 12-48
nitrite 3-30
false negative common for nitrites bc not all bacteria make them
- Do not rule out cystitis by a urinalysis that is negative for both leukocyte esterase and nitrites in the presence of a convincing clinical presentation
urine culture (find exact organism) only whne
antimicrobial resistance suspected
or in cystitis suspected in men
NOT uncomplicated cystitis
treat acute cysitits
1-5 days antibiotics if uncomplicated
7-14 days if complicated
symptom relief in 36 hours
asymptomatic bacteriruai
bacteria in urine without symtpoms
esp in old women
only screen or treat for asymptomatic bacteria if
pregnant (12-16 wk) (bc pre term birth) or getting a urologic procedure
recurrent cystitis
- 2 episodes of acute cystitis within the last 6 months, or
- 3 episodes of acute cystitis within the last year
do urine culture to see if recurrent or relpasign infection
pelvic exam for women nd rectal exam for men
**hygiene, increase fluid intake
atrophic vaginitis if estrogen decrease in menopause
acute pyeloneprhtitis
parenchyma of kidney
ascend for UTI
same KEEPS- esp e. coli
symptoms in pyelonephritis
rapid, dysuria, frequency, urgency, hematuria, fever, chills, N/V, flank or back pain, CVA
pyelonephritis on urinalysis
white blood cell casts
CBC
antibitotics for 7-14 days
send to hospital if pregnancy, unstable vitals, immunocompromsed
infectious urethritis
infection induce inflammation of uretha
usually from STI (esp homosexual male)
cause of infectious urethritis
80% gonococcal
2nd: chalmydia
STIs of the genitourinary tract manifest as urethritis in men and cervicitis in women
symptoms
dysuria, discharge , dyspareunia..
urethritis/ cervicitis from STI test
urine, PCR for gonorrhoea or chlamydia
urethritis from renters syndrome AKA reactive arthritis
autoimmune inflamamtory arthritis
from infection getting into genitals or bowel
swollen joints, urination burns
acute bacterial prostatis (men)
ascending urethral infection or intraprostatic reflux
from e coli (KEEPS) or gonorrhea
symptoms of acute abacterial prostatitis
fever, chills, vomit, low back pain, dysuria, painful ejaculation and defecation
test acute bacterial prostatitis
rectal exam
4 part urine culture VB1,2,EPS, VB3
support with antipyretics and stool softeners and antibiotics (4-6 weeks)
chronic bacterial prostates
irritative or obsrtuctuvie lower urinary tract symptoms etccccc
3-4 months of antibiotics
DDX of dysuria (pain when urine)
dermatologic, infectious, non infectious….
non inflam: endocrine, neoplastic, pscyhogenic///
CVA LR- is 0.9
useless - if not CVA then still might have kidney problem
dysuria further testing
- May not be required (e.g., in a woman presenting with uncomplicated UTI) – can treat empirically
or urinalysis…
Given the frequency with which peripheral vascular disease is asymptomatic, what percentage of patients is the Edinburgh Claudication Questionnaire targeted towards (pick the closest match)?
Question 1 Answer
a.
90%
b.
10%
c.
70%
d.
30%
maybe 10% idk
pseudodementiaa
depression or psych disorder alone or with dementia
dementia
major neurocogntiive disorder- cognitive decline, affect ADL, not delirium or depression
who’s likely to get demnetia
women old
most common dementia 70-80%
alzheimers
followed by FLTD 25%
strongest risk factor for demtnai
age
most common symptoms of dementia
memory impairmenta
agnosia
cant remember familiar things
aphasia
motor or sandy language disturbance
apraxia
cant do motor task
if :dementia” develops quick
be wary that its from infection or neoplasm etc
should be slow
1st step for dementia
history and phsycial exam
then mini cog then MMSE or MOCA then screen for depression, do labs and neuroimag
medications that impair cognition (dementia)
anticholinergics, sleep aids and anxiolytics, analgesics such as codeine containing agents
screening for dementia
USPSFT current evidence is insufficient to assess the benefits vs. harms of screening for cognitive impairment in older adults.
If dementia is suspected, physicians can use brief screening tests such as Mini-Cog then if abnormal do MOCA or MMSE
pseduodementia
- Psychiatric disease can lead to impaired cognition (pseudodementia).
- Clinical presentation: poor focus and concentration may primary complaint
labs for dementia
CBC, TSH, b12, metabolic panel
neuroimaging to rule out intracranial (MRI)
APOe4 gene testing
Genetic testing for apolipoprotein E4 allele is NOT recommended as part of the routine evaluation for cognitive impairment.
only if have family history
delirium
Acute confusional state that often occurs in response to an identifiable trigger
predisposing factors: depression, old, dementia, strokes, alcohol use
precipitation factrors: drugs, surgery, alcohol, metabolic coma
symptoms in delirium
inattention, reduced orientation to environmnet, hyper or hypo active
ACUTE
fluctuating course wax and wane in a day
delirium and dementia can coexist
need to resolve delirium then to diagnose dementia
Labs for delirium
CBC, chemistries, glucose, renal and liver function tests, urinalysis, test for occult infectio
MCI
A decline from a previous state of mental functioning that causes no or minimal interference with daily activities.
15% progress to dementia
- KEY feature differentiating MCI from dementia
Maintains level of function and capacity for independence in everyday activities
MCI reassess
annually to evaluate for progression to dementia.
non amnestic and amnestic MCI
amnestic= memory loss
MCI
evidence of lower performance in one or more cognitive domain
maintains preserved independence in functional abilities
change in cognition in comparison to the patient’s previous level.
alzheimers
amyloid plaques and neurofibrillary tangles
which allele of APOE is bad for AD
E4 (not E2 or E3)
vascular risk for dementia
Hypercholesterolemia, hypertension, diabetes mellitus, metabolic syndrome, obesity, and physical inactivity,
Around one-third of AD cases globally could be prevented by addressing modifiable vascular risk factors
!
AD presentation
most amnestic (memory)
nonamnestic: language, execute dysfunction, language impari
personality
depression
gait
imaging for AD
PET
CSF (amyloid an tau)
genetic testing
- Recommended for young patients with a history of first-degree relatives with young- onset dementia.12
* - APOE genotype is not recommended for routine evaluation of AD: most do not have the associated alleles, and current medical management would not change by the test results.
Diagnosing Alzheimer’s disease (AD) is challenging due to emotional responses from patients and families.
- Factors like coping mechanisms, culture, family dynamics, and existing knowledge impact reactions. Clinicians should be empathetic, honest, and provide resources for education and support.
- Goals include protecting memory, delaying progression, and ensuring safety.
- Use “Alzheimer disease” for diagnosis communication.
- Encourage local support groups and resources for effective patient management.
AD medications
cholinesterase inhibitors, NMDA receptor antagonists, and potentially aducanumab and other monoclonal antibodies targeting amyloid.
vascular dementia
Stepwise or progressive accumulation of cognitive deficits in association with repeated strokes.
risk factors for vascular dememtia
hyperlipidemia, hypertension, diabetes mellitus, and smoking (tobacco)
physical signs in vascular dementai
hemiparesis (one sided muscle weakness), pseudobulbar palsy and visual field defects
course of vascular dementia
Acute onset (following cerebrovascular event) of cognitive impairment with some stabilization (if only one vascular event) and/or stepwise deterioration (if multiple infarcts)
Lewy body dementia
alpha syncliun (lewy boes) in the cortex
Lewy body symptoms
attention and executive function,
hallucination, parkinson gait
NOT MEMMORY AS MUCH
other possible: REM sleep disorder, poor dopamine uptake
frontotemporal lobe dementia
- Behavior variant (bvFTD)
- Language variant:
- Non-fluent variant primary progressive aphasia (nfvPPA)
- Semantic variant primary progressive aphasia (svPPA)
risk for frontal temporal dementia
head trauma, thyroid disease, genes
FTLD presntiatia
decline in social cognition and/or executive abilities, but with relative sparing of learning and memory, and perceptual–motor function
BAD BEHAVIOUR- disinhibition**
loss of emotional reactivity, apathy
MEMORY INTACT UNTIL LATE IN DISEAE
FTLD biomarker in blood and CSF
neurofilmaent light chain
BEHAVIORAL AND PSYCHOLOGICAL SYMPTOMS OF DEMENTIA (BPSD)
agitation, depression, apathy
- cognitive/perceptual (delusions, hallucinations)
- motor (e.g., pacing, wandering, repetitive movements, physical aggression)
- verbal (e.g., yelling, calling out, repetitive speech, verbal aggression)
- emotional (e.g., euphoria, depression, apathy, anxiety, irritability)
- vegetative (disturbances in sleep and appetite)
Sundowning affects 2/3 of patients with dementia: behavioral disturbances often occur in the evening
whats suggestive of delirium
fever, hypoxia, abdominal tenderness, fluid overload, inflammation, or new localizing neurologic deficit
anemias
lower than normal level of healthy red blood cells or hemoglobin
- Characterized by low hemoglobin, low hematocrit, low RBC count on the complete blood count (CBC)
symptoms of anemai from decreased oxygen delivery to tisuse
fatigue, tachycardia, palpitations, dyspnea on exertion
best LR+ for anemai pallor
conjunctival rim
- Conjunctival rim pallor (LR+ 16.7) * Palmar crease pallor (LR+ 7.9)
- Palmar pallor (LR+ 5.6)
causes of anemia
reticulocytopenia- decreased RBC production
i..e DNA synthesis lesion (megaloblastic anemia), hemoglobin synthesis lesion (IDA)
reticulocytosis- increased RBC destruction (hemolysis) or accelerate RBC loss
i.e. spherocytosis, blood loss, cold or warm antibody, hypersplenism
acute blood loss
hypotension, tachycardia, ecchymose (bruising)
melena, hematemesis, hematuria, menorrhagia
low reticulocyte vs high reticulocyte
reticulocyte= immature RBC
low: RBC underpdorcution anemia
high: hemolysis or bone marrow response to blood loss
reticulocyte production index x
normal= 1
<2= hypoprofliferative anemia (underproduction)
> 2 = hyper proliferative anemia (hemolysis or blood loss)
MCV= average size of RBC
normocytic
macrocytic- subcategory of megaloblastic (impaired DNA synthesis) or non megaloblastic
microcytic
microcytic anemia in
iron deficency
thalassemia
anemia of chronic inflam (also normocytic)
normocytic
anemia of chronic inflam (could also be microyctic)
anemia of renal/kdiney disease
macrocytic anemia
megaloblastic: b12 or folate deficient
non-megaloblastic: myelodysplastic syndrome
non-megaloblastic macrocytic could be caused by
liver disease or hypothyroid
MCV
not specific
IDA
most common anemia
microcytic , hypochromic
causes: chronic blood loss, diet, impair absorb, increase demand..
IDA symptoms
restless leg, pica, glossitis, chelitis (tongue), koilonchia nails
best marker for IDA
decreased serum ferritin
also decrease transferrin, serum iron
increase TIBC
B12 deficiency anemia
megaloblastic macryoctic anemia (high MCV)
impairs DNA synthesis
lack intrinsic factor
metformin, PPI impair absorption
b12 deficiency anemia: pernicious anemia
autoimmune-mediatedgastricatrophy→lossofparietal cells→decreased secretion of intrinsic factor→decreased dietary vitamin B12 absorption
diagnose pernicious anemi
anti-intrinsic factor antibodies
tests in b12 deifciney anemia
low serum b12
high homocysteine
high methylmalonic acid MMA
folate deficiency anemia
qegalobasltic macryopcytic anemia (high MCV)
impair DNA synthesis
ddx of folate from b12 defiance anemia
in folate increased homocysteine but normal MMA in folate deficiency
both are high in b12
anemia of renal disease
kidney disease decreases EPO which decrease RBC
normcytic normochromic
low hemoglobin, low serum iron
2nd most common anemia
anemia of chronic disease (i.e. infection, inflame, malignancy, tumor)
anemia of chronic disease
impaired iron transport from iron storage sites (e.g., liver, spleen, bone
marrow) to developing RBCs→decreased production of RBCs
normocytic normochromic
increased iron stores, low serum iron,
other test for anemia of chronic disease
- Liver enzymes if there is history of liver disease
- Creatinine if there is history of kidney disease
- Elevated inflammatory markers: ESR and CRP
basic metabolic panel to see if chronic kidney disease
Glucose
* Calcium
* Sodium
* Potassium
* Carbon dioxide
* Chloride
* Blood urea nitrogen (BUN)
* Creatinine
then look at GFR
most common inherited disoders
thalassemias
thalasssmeia
Congenital abnormality of hemoglobin synthesis → decreased production of RBCs
alpha or beta
4 missing Alpha gene
hydros fatalis
3 missing alpha genes
hemoglobin h disease
symptoms in moderate to sever thalamsemia
includes β- thalassemia intermedia, β-thalassemia major, and Hemoglobin H disease
- Severe anemia
- Growth disturbances and delayed puberty
- Bone abnormalities (e.g., osteoporosis)
- Splenomegaly
- Pallor or jaundice
mild thalassemia
hypo chronic and microcytic anaemia may have splenomegaly
very mild
diagnose thalassemia
look at family history of anemia
CBC, hemoglobin electrophoresis, genes
myelodysplastic syndrome
aka hyperplastic bone marrow with bone marrow failure, refractory anemia, smoldering leukemia, preleukemia
Blood cell components fail to mature → deficient production of mature cells into peripheral blood (including RBCs)
5 types of myelodysplastic syndrome
- Refractory anemia
- Refractory anemia with excess blasts
- Refractory anemia with leukemia in transformation
- Refractory anemia with sideroblasts
- Chronic myelomonocytic leukemia
can transform into leukemia in certain time frames
myelodyspalstic syndrome presentation
megaloblastic or microcytic anemia
pancytopenia: anemia with abmnormalieties in 1 or 2 of other marrow cell lines (WBCs, platelets)
hemolytic anemia
normocytic
caused by RBC destruction
inherited (i..e sickle cell) or acquired (i.e. infection)
extravascular vs intravascular hemolytic anmie
extravascular- RBC prematuelry removed from circulation by liver and spleen (MAJORITY)
intravascular: RBC lysed in circulation
symtoms of hemolytic anemia
SOB, fatigue, tachycardia, jaundice, lymphadenopathy, hepatosplenomeagly
diarrhea
hematuria
- Hemolytic anemia with diarrhea → consider hemolytic uremic syndrome
- Hemolytic anemia with hematuria → consider paroxysmal nocturnal hemoglobinuria
x
tests for hemolytic anemia
- Elevated reticulocyte count
- Increased lactate dehydrogenase (LDH)
- Elevated unconjugated bilirubin
- Decreased Haptoglobin
Coombs: cold or warm agglutinin (immune)
spherocytes, bite cells
untreatmed anemia
in pregnancy premature, low birth weight
elderly: cardiac complication
kids: neurolgoical development
A naturopathic doctor receives lab results for their patient who has fatigue, the results of which indicate a macrocytic anemia. What is the most appropriate differential diagnosis?
Question 3 Answer
a.
Kidney disease, copper deficiency, zinc deficiency
b.
Vitamin B12 deficiency, hypothyroidism, liver disease
c.
Anemia of chronic inflammation, copper deficiency, myelodysplasia
d.
Aplastic anemia, lead toxicity, thalassemia
B
What lab result should most increase a naturopathic doctor’s estimate for the probability of anemia?
Question 4 Answer
a.
Low hemoglobin
b.
High RDW (red cell distribution width)
c.
High MCV (mean corpuscular volume)
d.
Low ferritin
A
how many headaches are life threatening
< 1%
findings for secondary headaches on physicals
focal neurological deficits, papilledema, bitemporal hemianopia, homonymous hemianopia, decreased visual acuity, or increased pain with Valsalva method
new headaches
- recent onset or
- chronic headaches that change character/qualitty
headache changes
- Change in severity is less important than change in quality
most common primary headaches
migraine and tension type
most new headaches are
benign but almost all serious headaches are new
primary vs secondary
primary: tension-type headache, migraine headache, cluster headache ( no underlying caused) (no labs or imaging as gold standard)
secondary from other thing (i.e. infection, vascular, temporal arthritis, URTI, TMJ, cervical degeneration, brain tumor )
are most headaches primary or secondary
primary
worrisome headaches
new and secondary
SNNOOP10 for red flags in headache
systemic
neoplasm
neurlogic
onset
old
Pattern, positional, preceiptatied, papilledema, progressive or atypical presentation, pregnancy, painfulful eye, post trauma, painfkiller
highest LR for red flags in headaches
disequilibrium (49)
headache causing awakening from sleep (1.7-98)
neuroimaging in headache
if have red flag
(new and sudden onset severe, >50 yrs old, HIV, associated with neurologic deficits)
pretest probability for severe intracranial pathology
thunderclap headache 43%
predict neuroimaging abnoramlities
cluster type headache LR+ 11
(they’re primary and benign but symptoms overlap with serious headaches)
abnormal neurological 5.3
difficult to classify and not a primary ehadaachees 3.8
MRI, CT with or without contrast
CT if trauma and hemorrhage
otheer if progressive worse
lumbar puncture for headache
infection, RBC, xanthochromia (yellow CSF from bilirubin)
do if have: meningeal sign, HIV, altered mental status, neurological deficits
labs for headache
CBC (infection)
ESR and CRP (temporal arteritis)
metabolic panel
endocrine (pituitary)
rhinosinusitis and headache
bacterial or viral infection of sinus an dnsal–> facial pain, pressure
high LR+ symptoms after URTI, if Dr thinks it is
better in 7-10 days
do antibiotics
meningitis
headaches, fever, stiff neck, alter mental status
viral (common) or bacterial (more fatal)
acute, rapid onset
meningeal sings
- Kernig sign (resistance to knee extension with hip flexion)
- Brudzinski sign (involuntary hip flexion with neck flexion)
- Nuchal rigidity (resistance to neck flexion)
- Jolt accentuation of headache (worsening of headache by horizontal rotation of the head).
bacterial meningitis 95% sensitivity
2 of: headache, fever, stiff neck, mental status change
diagnose meningitis
CSF from lumbar puncture
head trauma
minor in 90% (glasgow coma scale)
symtoms: loss of consciousness, amnesia, headache
CT for minor head truma LR+
physical exam findings suggest skull fractures (16)
GCS score of 13 (4.9)
skull fracture findings
CSF otorrhea, periorbital ecchymosis (racoon eye), hemotympanum (ear drum), postauricalualr echymosis (battle sign)
mild TBI
headache mint to hour and days to weeks after even
early: fatigue, dizzy nausea
late: anxiety, concentrating, sleep, light sensitive
head trauma testing
CT
subarachnoid hemorrhage
blood vessel rupture btw space in brain and skull
WORST HEADACHE OF LIFE
vomit, neck stiff, lose consciousness
risks for subarachnoid hemorrhage
cigarettes, hypertesnion, old man
type of headache in subarachnoid hemorrhage
thunderclap headache (abrupt and max intensity usually with vomiting)
warning “sentinel” headache
subarachnoid hemorrhage testq
non constrast CT then lumbar puncutre if needed (xanthochromia)
idiopathic intracranial hypertension
severe daily headaches in young obese women (chronic)
may awaken from sleep
associated with visual disturbance
symptoms in idiopathic intracranial hypertension
chronic headache and progressive visual deterioration
90% finding in idiopathic intracranial hypertesnion
papilledema
12% of times in idiopathic intracranial hypertension
CN6 palsy
test in idiopathic intracranial hypertesnion
increased ICP
normal MRI or CT
prognosis of idiopathic intracranial hypertesnion
vision loss
temporomanidcular disorder headahce
TMJ cause headache and facial pain when chew
esp women
jaw sounds, jaw mobilitiy
signs for TMJ headahce
facial pain 96%
ear discomfit 82%
headache 79%
jaw discomfort or dysfunction 75%
brain tumors
primary or metastatic
metastatic 7x more common (lung 37%, breast, melanoma)
progressive headache
headache, worse in morning, N/V, alter mental status, weak
neurological exam in brain tumor
hemiparesis (one sided muscle weak), impaired cognition, sensory loss, gait abnormalities
symptoms for brain tumor
headache, seizure,
anosmia, apraxia, cognitive delay, drowsiness, dysphagia, hallucinations, memory loss, nausea and vomiting, pain, and stiff neck
primary brain tumors have different manifestationn depending on location
i.e. thalamus has behavioural dn language change
front lobe has dementia, gait, sensory loss
brain tumor test
MR then CT
medication over use headache
from analgesics
highest risk: opioids, triptans, ergotamines, NSAIFs and acetominaphrin
one of the most common secondary headaches
more in women, low SES
associated with chronic migraine or tension type headache
time course of medication overuse headahce
> 15 headaches/ month for 3 months of medication use
take the drugs for 10-15days/month
symptoms in medication overuse headache
neck pain, sleep, GI, anxiety/depress, autonomic (rhinorrhea)
temporal arteritis
> 50 years old with jaw claudication
esp if have poly myalgia rheumatica
LR+ for temporal arteritis
scalp tenderness and jaw claudication 17
headahce and jaw claufidation 8
test for temporal arteritis
gold standard- temporal artery biopsy
ESR
prognosis of temporal arteritis
could go blind
primary headaches
tension-type headaches, migraines, and cluster headaches
short <4 hours (cluster, stabbing, SUNA, SUNCT)
long> 4 hours (migraine, tension)
if no red flags dont need imaging for primary headaches
just history and physical exam
cluster headache
unilateral and cluster in time (brief 15-180 min, up to 8 episode a day)
90% episodic (remission for 1 month)
young men
autonomic + restless
symptoms of cluster headache
rapid onset, in retro orbital area or temporal region
unilateral
autonomic: congestion, eyelid edema, sweat forehead, lacrimation
restless and agitated 90%
clusteheadache testing
yes, neuroimagin bc LR=11
comobrid in cluster headache
depression, sleep apnea, restless leg, astham
Short-lasting Unilateral Neuralgiform Headache (SUNCT or SUNA)
trigmeinal nerve stimuli
1 second- 1o mins
unilateral pain
autonomic: eye edema, lacrimation, rhinorrhea, forehead sweat
SUNA vs SUNCT
SUNA
either lacrimation or conjunctival injection but not both
SUNCT
both lacrimation and conjunctival injection
primary stabbing headaches
shortest lasting; 3 seconds
42% temporal region; can change location
no autonomic symptoms
migraine
chronic, unilateral pulsating headache with nausea, photophobia, phonophobiaa
possible aura (60 min)
4-72 hours
most common primary headache
- tension
- migraine
migraine symptoms
pulsating or throbbing pain, bilateral 60% (or uni?)
nausea, photophobia, photophobia
worse with stress, menstrual, nitirite or tyramine in foods, fatigue
auras in migraines in 1/3 of patients
<30 mins (70%) and stars of flashes (83%) or zig zags (56%)
blind spot then falshing light
migraine screening tool if have score of 2 or 3 its LR+ 3.25
2 and 3 have good LR-
- Nausea: “Did you ever feel nauseous when you had headache pain?” (BEST LR+ OF 3.2 alone)
- Photophobia: “Did light trouble you when you had headache pain (much more than when there was no headache)?”
- Disabling Intensity: “Did your headache ever limit your ability to work, study or do something you needed to, for at least 1 day?”
risk for episodic to chronic migraine
if frequent, medication overuse, obese, diabetes, arthritis, head or neck injiury
tension type headache
most common
worse withs tress and end of day
symptoms of tension headache
bilateral pressure (pressing/ non pulsing)
migraines are
PULSITLE (tension type are not)
migraines can be worse qith
chocolate, cheese, phsycial activity
POUND for migraine
- Pulsatile quality
- Duration of 4 - 72 hOurs
- Unilateral location
- Nausea or vomiting
- Disabling intensity
if 4-5 of these then LR+ 24
chronic headaches
> 15 headaches / month for 3 months
usually migraine or tension or medication overuse
other risks
* Chronic pain, especially musculoskeletal pain * Cutaneous allodynia
* Sleep disorders
* Obesity
* High caffeine consumption
* Stressful life events, especially in middle age
chronic migraine
- May evolve from episodic migraine
- Patient typically report progressively frequent bilateral frontotemporal TTH-type symptoms with superimposed full- blown migraine attacks
- Comorbidities: obesity, obstructive sleep apnea, depression, chronic pain disorders, cardiovascular disease, sleep and emotional disturbances
chronic tesnsion type
- Long attack duration and nausea are predictive of development of chronic TTH
- Bilateral, non-pulsatile, absence of associated symptoms * Pericranial tenderness is often found on palpation
headache impact test (how you feel)
headache diary
PHQ9, CAGE
x
A 32-year-old man presents with concerns of a rapid-onset, severe headache with mild neck stiffness which started while performing pushups 2 hours ago. He has no other known illness. On physical examination, there are no neurological abnormalities. The naturopathic doctor considers tension headaches to be a likely diagnosis. What other differentials should they consider?
Question 1 Answer
a.
Primary thunderclap headache and exercise-induced migraine
b.
Subarachnoid hemorrhage and primary exercise headache
c.
Primary stabbing headache and cluster headache
d.
Cervicogenic headache and headache attributed to fasting
B
A naturopathic doctor has seen the following pediatric patients regarding their headaches.
PA. a 2-year-old girl
QB, a 7-year-old boy
RC, a 9-year-old boy
SD, a 14-year-old girl
Which of them was most likely to be experiencing migraines?
Question 3 Answer
a.
PA
b.
SD
c.
QB
d.
RC
B
What aspect of patient-centered interviewing is particularly applicable to initiating an interview with a patient experiencing headaches?
Question 5 Answer
a.
Use the patient’s name, in case confusion is a symptom associated with the patient’s headaches
b.
Ensure patient readiness and privacy, since patients are often embarrassed about the cause of their headaches (e.g. headaches associated with sexual activity)
c.
Understand the patient’s agenda, since patients often seek medical care for headaches when they are concerned about serious diagnoses
d.
Attend to non-verbal cues such as autonomic changes which may be present in migraine auras or cluster headaches
C
