Syncope and Fatigue DSAs Flashcards Preview

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Flashcards in Syncope and Fatigue DSAs Deck (40)
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1
Q

Vertigo

A

false sense of motion or spinning

2
Q

Presyncope

A

prodromal sx of fainting or near fainting

no LOS, often described as tunnel vision

3
Q

Syncope

A

clinical syn w/ transient loss of consciousness

4
Q

disequilibrium

A

sense of imbalance primarily when walking

5
Q

HOlter monitor

A

Continuous ambulatory ECG worn for 24-72 hrs

pt can press button and mark ECG when they feel sx

6
Q

Event (loop) monitor

A

ECG that continuously loops its recording tape

pt triggers devise to record when sx arise

worn for weeks to months at a time

7
Q

What does a tilt-table test help with?

A

diagnosing vasovagal syncope, orthostatic hypotension, etc

8
Q

What are the 3 major types of syncope?

A

cardiac = 20%

reflex = neurally-mediated; vasovagal; 60-70%

orthostatic hypotension syncope = 10-20%

9
Q

What are the 5 types of orthostatic hypotension syncope?

A

drug induced

postural thacycardia syndrome

primary autonomic failure (neuro stuff)

secondary autonomic failure (chronic systemic syndromes)

volume depletion

10
Q

What characterizes hypertrophic cardiomyopathy?

A

left vent hypertrophy w/out clear secondary cause

most cases from genetic mutations (AD)

most pts have no sx or only minor sx –> can have presyncope or syncope, particularly during or immediately follwoing exertion

can have arrhythmias or SCD

11
Q

What does HCM sound like?

A

S4 may be present

systolic murmor

*squatting increases intensity of all murmors except mitral valve prolapse and HCM

valsalva and standing increase MVP and HCM

12
Q

What increases the sound of HCM?

A

valsalva

standing

(NOT sustained handgrip)

13
Q

How is HCM diagnosed?

A

family hx or genetic testing

LV wall 15 mm or more on echo

LVOT obstruction is present

14
Q

What is the tx plan for HCM?

A

avoid strenuous activity

asymptomatic –> no further tx

Beta blockers or non-dihydropyridine CCBs

diuretics (w/ caution)

ICDs

surgery for severe cases

15
Q

What are the 2 main surgeries for severe HCM?

A

myomectomy

alcohol ablation –> infarct proximal interventricular septum

16
Q

What cause of syncope has the worst outcome?

A

cardiac cause

50% mortality at 5 yrs

17
Q

what are the 3 main types of reflex syncope?

A

carotid sinus hypersensitivity and syn: triggered by stim of carotid A baroreceptor from mechanical forces, seen in old men w/ atherosclerosis

situational syncope: triggered by micturition, defecation, sneezing, etc

vasovagal: prolonged sitting or standing, emotional stress or fear, pain, heat

18
Q

How do autonomic failure pts present?

A

have supine hypertension

hypotension when upright

19
Q

What defines orthostatic vital signs?

A

drop of 20 mm hg systolic or 10 diastolic w/in 5 min of standing

20
Q

What is POTS?

A

postural tachycardia syndrome

form of orthostatic intolerance in response to postural changes

autonomic reflexes are preserved, but there is an exaggerated increase in HR w/ position chgs –> redist of blood –> reduced cerebral flow

no hypotension present on tilt table test

21
Q

What are the tilt table results in POTS?

A

sustained HR incr > 30 bpm or an absolute hr > 120 bpm w/in first 10 min of tilt

NO hypotension

22
Q

What are 4 inherited risks of PE?

A

factor 5 leiden mutation

prothrombin mutation

protein C or S def

anti-thrombin deficiency

23
Q

What oral anticoagulants are preferred for PE tx?

A

factor Xa inhibitors (rivaroxaban, apixaban, edoxaban)

direct thrombin inhibitors: dabigatran

warfarin

24
Q

What subcutaneous anticoagulants are used in tx of PE?

A

LmWH (preferred in pt w/ malignancy, avoid in renal failure)

fondaparinux

25
Q

What is the preferred anticoagulation tx plan for PE?

A

DOACs

warfarin if contraindication fo DOACS or renal impairment

LMWH preffered agent in pt w/ underlying malignancy or pts that can’t take oral meds

26
Q

How long is anticoagulation therapy after a PE?

A

3 months min

low to mod risk of bleeding –> extend

high bleeding risk –> only 3 mos

27
Q

What do osmoreceptors sense and where are they?

A

in anterior hypothalamus

sense increases in serum osmolality –> release ADH

28
Q

What do baroreceptors and atrial stretch receptors sense?

A

decreases in Bp or increases in blood volume –> manage ADH release

29
Q

What does ADH do to the collecting duct?

A

binds V2 receptor –> AQP-2 inserted into collecting duct –> reabsorb more h2o

30
Q

What can cause nephrogenic DI?

A

hereditary seen in children

lithium toxicity

hypercalcemia

hypokalemia

other renal dzs

31
Q

How do you diagnose DI?

A

24 hr urine volume collection

urine osm < 300 mOsm/kg

water deprivation test –> see if urine concentrates or not

32
Q

How do you tx nephrogenic DI?

A

decreased solute intake

thiazide diuretics

NSAIDs

Vasopressin

33
Q

What are 5 important non-osmotic stimuli for ADH release to know?

A

baroreceptors

nausea

hypoxia

pain

medications (opiates, antipsychotics and antidepressants)

34
Q

what defines hyponatremia?

A

serum sodium < 135 mEq/L

results primarily from increases in total body water

35
Q

What do you see on ECG in left ventricular hypertrophy?

A

huge T waves in left ventricle leads

deep S or R waves on LV leads

36
Q

What will urine and serum be like in SIADH?

A

will have urine w/ too much sodium (not reabsorbing enough)

hypo-osmotic serum

low serum uric acid is associated w/ SIADH as urid acid exretion is high in the urine

37
Q

If evaluating hyponatremia, when should you run labs?

A

simultaneously

38
Q

How would you treat SIADH?

A

free water restriction < 1000 ml/day

give salt tablets

stop diuretics

39
Q

How often should you measure pt’s serum sodium level when treating SIADH?

A

every 2 hours

40
Q

How do you measure the severity of OSA?

A

mild: AHI 5-15 events/hour
moderate: 15-29 events/hour
severe: 30 or more events/hour