ED Rotation

Question 1

Anterior Cord Syndrome

Answer 1

• Flexion or vascular cause
• complete loss of motor, pain, and temperature below lesion
• proprioception and vibratory sense intact
• **this has worse prognosis

Question 2

Central Cord

Answer 2

• Forced hyperextension = mechanism
• sensory and motor deficits, upper > lower

Question 3

Brown Sequard Syndrome

Answer 3

• mechanism = penetrating
• ipsilateral vibratory, motor and proprioception loss
• contralateral loss of pain and temperature
• **This has best prognosis

Question 4

Definitions: Sepsis, Systemic Inflammatory Response Syndrome, Septic Shock

Answer 4

• Sepsis:
  
  • life-threatening organ dysfunction secondary to dysregulated host response to infection
    
    • condition
• Systemic Inflammatory Response Syndrome (SIRS):
  
  • an exaggerated defense response of the body to a stressor (infx, trauma, surgery, acute inflammation, ischemia, etc). meant to localize and then eliminate the source of the insult
• Septic Shock:
  
  • a subset of sepsis in which particularly profound circulatory, cellular, and metabolic abnormalities are associated with a greater risk of mortality than with sepsis alone.

Question 5

SIRS Criteria

Answer 5

Systemic Inflammatory Response Syndrome is defined as presence of 3+ of the following”

• fever > 38C (100.4F) or hypothermia <36F (96.8F)
• Tachypnea (RR > 24)
• Tachycardia (HR > 90/min)
• Leukocytosis (>12K), Leukopenia (<4K), or >10% bands

Question 6

Sepsis vs Severe Sepsis

Answer 6

• Sepsis:
  
  • at least 3 SIRS criteria AND a confirmed or suspected infection
• Severe Sepsis:
  
  • sepsis WITH evidence of end-organ damage due to the tissues not getting adequate perfusion
    
    • hypotension
    • serum lactate levels (≥ 4.0mmol/L)
    • pre-renal azotemia and transaminitis (elevated ALT/AST)

Question 7

Hour-1 Sepsis Bundle

Answer 7

Question 8

Exam findings of Septic Shock

Answer 8

• Compensated:
  
  • tachycardia
  • dynamic (heaving) precordium
  • bounding peripheral pulses
  • reduced cap refill
  • skin = warm or hot to touch (WARM shock)
• Decompensated Septic Shock:
  
  • peripheral pulses become weak/thready
  • hypotension worsens
  • skin becomes cold/pale/clammy (COLD shock)

Question 9

Management of Septic Shock

Answer 9

• fluid resuscitation with Crystalloid (NS or albumin) and colloid (blood products) up to 80ml/kg
• 1st line vasoactive agents for fluid refractory shock:
  
  • Norepi in Warm shock (compensated)
  • Epi in Cold Shock (decompensated)
• add vasopressin if refractory to vasopressors
• Restore MAP to ≥ 65 mmHG
• Restore Central venous pressure (CVP) to 8-12mmHg

Question 10

How to Calculate MAP

Answer 10

Mean Arterial Pressure

• MAP = [(Diastolic BP x 2) + Systolic BP] / 3

Question 11

ABA Burn Center Referral Criteria

Answer 11

Question 12

Burn Treatment

Answer 12

• Keep the patient warm, prevent hypothermia
• < 15% BSA burns
  
  • moist sterile dressing
• >15% BSA burns
  
  • cover with dry sterile dressing
    
    • decreases risk of hypothermia
• for bigger areas → use a clean dry sheet

Question 13

Parkland Formula for fluid resuscitation in a burn patient

Answer 13

• IV fluid of choice = Ringer’s Lactate
• 1st 24 hours:
  
  • 4mL x kg x % BSA burned
  • 1st 8 hours: give ½ of total fluid
  • next 16 hours: give rest of fluid (½ of total fluid)
• Inhalation Burn: 6ml x kg x % BSA
• Electrical Burn: 7ml x kg x % BSA

Question 14

Airway & Breathing Tx for Burn Patients

Answer 14

• >15% BSA burns: give 100% oxygen even if pulse ox is normal
• Be prepared to support ventilation
  
  • may require an advanced airway for inhalation burns

Question 15

Rule of 9s

Answer 15

Question 16

Superficial vs Partial Thickness vs Full Thickness

Answer 16

• Superficial:
  
  • epidermis only
  • pain & erythema
  • heals in a few days
    
    • topical aloe vera
    • injured epidermal cells peel away
• Superficial Partial Thickness:
  
  • entire epidermal & superficial (papillary) dermis
  • erythematous & skin may blister
    
    • may be moist, weepy, or shiny
    • painful & hypersensitive to touch
  • blanches with pressure
    
    • does not extend into capillary bed so it can heal better b/c basement membrane is intact
  • usually heals on its own in 2-3 weeks
• Deep Partial Thickness:
  
  • extends into deep (reticular) dermis
  • Blood filled blisters
  • usually Mottled pink to white in color
  • Does NOT blanch
  • healing time = 3+ weeks
    
    • may require excision and skin grafting
• Full thickness:
  
  • total loss of dermis & epidermis
  • Skin appears dry, leathery, peeling
    
    • may be white, yellow, tan/brown, or charred
    • hair follicles removed easily
  • often not painful
  • may require escharotomy or fasciotomy
  • heals by contracture & epithelial ingrowth or skin grafting

Question 17

Categories of Shock Table

Answer 17

Question 18

Stages of Shock

Answer 18

Question 19

T or F : a normal BP rules out shock

Answer 19

FALSE, a normal BP does NOT rule out shock

Question 20

What are 3 identifiable and treatable immediately life-threatening causes of shock?

Answer 20

• Bleeding
• Tension Pneumothorax
• Pericardial Tamponade

Question 21

What would you use tranexamic acid for?

Answer 21

it is an antifibrinolytic

helps to stabilize the clotting system during hemorrhagic shock

Question 22

what is the MCC of cardiogenic shock?

Answer 22

Acute MI

Question 23

Tx of Cardiogenic Shock

Answer 23

Question 24

Types of Distributive Shock

Answer 24

Question 25

Neurogenic Shock Overview

Answer 25

Question 26

Anaphylactic Shock

Answer 26

Question 27

Obstructive Shock Overview

Answer 27

Question 28

EMTALA

Answer 28

Emergency Medical Treatment & Labor act of 1986

requires hospital EDs to medically screen all pats who present requesting care for an emergency medical condition

CANNOT be screened by a triage RN

Question 29

Advantages and Limitations of Transfers via Private Car, Wheelchair/Gurney Van, BLS, ALS, and CCT

Answer 29

Question 30

Advantages and Limitations of Transfers via Specialty Teams, Heli, Fixed Wing

Answer 30

Question 31

Hypothermia Body Temps

Answer 31

Body Core Temp < 35C (95F)

• Mild Hypothermia: 32-35C (90-95F)
  
  • shivering, increased metabolic rate, conscious to mildly AMS, ability to self rewarm
• Moderate Hypothermia: 28-32C (83-90F)
  
  • AMS, ECG changes (J wave–right after QRS complex) loss of shivering at 30C (86F) losing ability to self-rewarm
• Severe Hypothermia: <28C (83F)
  
  • decreased metabolic rate by 50%, not shivering, unconscious, lowered threshold for dysrhythmias (VF/VT), incapable of self-warming

Question 32

Afterdrop and Hypothermia

Answer 32

• Occurs after the cooling process has been stopped
• when heat from the core gets conducted to the circulation and the periphery
• expect the body temperature to drop an additional 1.3-6.4C
  
  • patient may get worse before they get better after being removed from the cold

Question 33

General Tx of the Hypothermic Patient

Answer 33

• remove pt from cold
• administer oxygen (warmed and humidified)
• assess for other injuries & illnesses
• check blood sugar
• hand gently – avoid rough and excessive movement
• anticipate afterdrop

Question 34

Tx of Mild Hypothermia

Answer 34

• Assess LOC and gag reflex
• provide warmed oral fluids with calories
  
  • no caffeine, alcohol, or nicotine
• passive rewarming
• external heat (if possible)
• may not require further treatment

Question 35

Tx of Moderate Hypothermia

Answer 35

• Assess for pulse & respirations for at least 60-120sec
  
  • if respirations or cardiac electrical activity are present, assume cardiac output, even if a pulse is not present
  • U/S can be used to detect cardiac activity
• active external rewarming
• IV/IO access:
  
  • fluid bolus with warmed NS (40-42C [104-107F])

Question 36

Cardiac Arrest in Hypothermia

Answer 36

• If VT/VF is present or AED advises shock, defibrillate once at max output
• start CPR
• ventilate with warmed oxygen
• hypothermic heart does not respond well to ACLS meds as drug metabolism will be reduced
  
  • withold ACLS meds for core temps < 30C (86F)

Question 37

Active vs Passive Rewarming of Hypothermic Patients

Answer 37

• no shivering in a hypothermic pt?
  
  • active rewarming recommending
    
    • large heat packs/hot water bottles
    • forced warm air
    • invasive/extracorporeal warming (ECMO, bypass machine, etc)

Question 38

Define & Tx Heat Exhaustion

Answer 38

• Definition:
  
  • Flu-like sxs:
    
    • malaise, HA, weakness, pale skin, loss of appetite, nausea & vomiting
  • tachycardia, orthostatic hypotension
  • temp usually around 38-39C (100.4 - 102.2F)
  • sweating
  • normal mental status
• Tx:
  
  • cooling measures
  • oral fluids
    
    • dilute sports drinks (½-⅓ strength)
    • cooler fluids are more easily absorbed
  • Oxygen as necessary
  • they may be able to self-evacuate after cooling and rehydration

Question 39

Define & Tx Heat Stroke

Answer 39

• Definition:
  
  • Body temp us usually 104F (>40C)
  • AMS = most important!
    
    • confusion, bizarre behavior, loss of balance, seizures, coma
  • hypotensive, tachypnic, tachycardia
  • flushed, red skin
  • sweating +/-
• Tx:
  
  • aggressive cooling measures
    
    • wet clothing/sheets, fans, ice water baths, ice/cold packs on armpits, neck and groin
  • Protect the airway
  • Monitor body core temp

Question 40

Exercise Associated Hyponatremia

Answer 40

• athletes who exercise in hot weather
• consume excess amounts of water or hypotonic fluids
  
  • dilution hyponatremia (usually <125 mmol/L)
  • weight gain
• Neuro sxs
• Rapid serum Na+ measurement is crucial
• Tx is sodium repletion (IV 3% NaCl)

Question 41

Snake Bites: Local Rxn, Systemic Rxns, Tx

Answer 41

• Local Reaction:
  
  • Pain, swelling, discoloration, numbness, paresthesias, hemorrhagic blebs
• Systemic Rxns:
  
  • diaphoresis, chills, weakness, metallic/minty taste
  • neurologic sxs:
    
    • paresthesias of tongue, mouth or feet
    • fasciculations in face, back and neck
  • Anaphylaxis
• Tx:
  
  • Calm victim, remove constricting clothing/rings/etc, assess for signs of bite, measure and mark swelling
  • cleanse area around bite with soap and water
  • immobilize at heart level
  • establish IV access (2 lines: 1 for antivenom, 1 for fluids
  • Draw labs:
    
    • CBC, PT, PTT, fibrinogen, D-Dimer, CMP, CK, troponin-I, UA, type and screen
  • Give Antivenom
  • All pts should be observed for 18-24 hours
    
    • generally require ICU admission

Question 42

Tick Paralysis: s/sxs & Tx

Answer 42

• presents similarly to guillain barre
  
  • progressive, ascending, symmetric, flaccid paralysis with loss of DTRs
    
    • caused by a neurotoxin transmitted by the bite of a female Dermacentor tick
      
      • sxs usually begin 5-6 days after tick has initially attached
• Tx:
  
  • tick removal, supportive care, ventilatory support until the sxs resolve
  • no antivenom available

Question 43

Major Risk Factors for Falls

Answer 43

• female gender
• older age
• hx of previous fall(s)
• extremity weakness
• psychotropic med use
• co-morbidities (Parkinsons, cardiac disease, infection)

Question 44

Canadian CT Head Rules

Answer 44

• Do any of the following apply?
  
  • GCS < 15 at 2 hours after injury
  • Suspected open or depressed skull fracture
  • vomiting ≥ 2 episodes
  • Age ≥ 65 years
  • Pre-impact amnesia ≥ 30 minutes
  • Dangerous mechanism
• If yes to any -→ CT required!!

Question 45

New Orleans Head Trauma Rule

Answer 45

• Do any of the following apply?
  
  • HA
  • Vomiting
  • Age > 60 years
  • Alcohol or drug intox
  • Persistent anterograde amnesia
  • visible trauma above the clavicles
  • seizure
• if yes to any → CT is indicated

Question 46

The Disaster Cycle

Answer 46

• Planning
• Preparedness
• The Disaster Event
• Response
• Recovery/mitigation
• Planning (Again)

Question 47

What does START stand for in disasters?

Answer 47

Simple Triage and Rapid Treatment

Question 48

ACLS Medications

Answer 48

Question 49

Respiratory Failure vs. Respiratory Arrest

Answer 49

Question 50

Anaphylaxis Criteria

Answer 50

Question 51

Tx of Anaphylaxis

Answer 51

Question 52

Tx of Anaphylactic Shock

Answer 52

• Volume resuscitation (2-7 L) for persistent hypotension
  
  • NS > LR
• Epi infusion
• Dopamine/Dobutamine for refractory shock
• Glucagon for pts on beta-blockers → to reverse the beta blockade
• endotracheal intubation and mechanical ventilation

Question 53

Biphasic Anaphylaxis

Answer 53

• Anaphylactic rxns are typically uniphasic and resolve in an hour
  
  • some episodes may last hours - days
• up to 23% may experience return of sxs in hours to days (biphasic rxn)
  
  • typically less severe than initial rxn
  • almost all cases are not clinically significant and there are no fatalities
    Can use methylprednisolone to attempt to prevent biphasic pattern

Question 54

Anaphylaxis: Observation, Discharge and Pt Ed

Answer 54

• Mild - moderate anaphylaxis with complete resolution of sxs:
  
  • observation recommended for 4-8 hours
  • if pt remains asymptomatic, consider a short outpt course of H1/H2 blockers and glucocorticoid therapy
  • all pts need to be discharged with an epi pen
• All pts without complete resolution of sxs or requiring an infusion of meds should be admitted for further observation

Question 55

Correction Factor for Sodium in DKA

Answer 55

• Add 1.6mEq Na for every 100mg/dL the glucose is above normal

Question 56

Tx of DKA

Answer 56

• ABCs
• IV Fluids:
  
  • 20-30cc/kg of crystalloid
  • LR is best b/c it is closer to physiologic solution and does not cause hyperchloremic metabolic acidosis
• Electrolyte Correction:
  
  • Potassium = most important lab
    
    • Oral: KCl 40mEq q hour
    • IV: KCl 10-40 mEq in each liter of fluid
    • Insulin will push potassium intracellularly so watch it!!
    • hypokalemia = hypomagnesemia → replace Mg → 1-2 gm MgSO4 IV
  • Sodium: dilutional hyponatremia will correct on its own
• Insulin:
  
  • insulin should NOT be started until K+ level is known
    
    • Regular (Humalog/Novalog) Insulin infusion 0.1-0.4 units/kg/hr
    • do NOT bolus, can be harmful
• Bicarb:
  
  • only if pH < 7.1
    
    • pt needs to be able to blow off CO2 → ventilatory rate must be artificially increased
    • watch out for: hypokalemia, delay in improvement of ketosis

Question 57

Tooth Anatomy

Answer 57

Question 58

Local Analgesics for Dental Pain

Answer 58

Question 59

Pediatric Assessment Triangle

Answer 59

Appearance

Breathing

Circulation

Question 60

When to refer to ophtho

Answer 60

Question 61

When to refer to ENT with epistaxis

Answer 61

Question 62

Recommended Screening for DM II

Answer 62

Question 63

Bishop Score and Cervical Favorability

Answer 63

Question 64

Which medications are involved in dual antiplatelet therapy?

Answer 64

• Aspirin: impairs platelet aggreggation via inhibition of thromboxane A2 synthesis, COX inhibitor
• P2Y12 inhibitors: clopidogrel, inhibits platelet aggregation

Question 65

Anisocoria

Answer 65

asymmetric pupil

can be variant or pathological

Question 66

Left vs right Visual Field Processing

Answer 66

Question 67

myopia

Answer 67

impaired distance vision

• impaired distance vision
  
  • aka “nearsightedness”
  • when you have an elongated eyeball
    
    • treated with a concave lense

Question 68

Hyperopia

Answer 68

impaired near vision

• “farsightedness”
  
  • when you have a short eyeball
    
    • treated with a convex lense

Question 69

presbyopia

Answer 69

• type of hyperopia (loss of near vision) due to aging

Question 70

emmetropic

Answer 70

normal vision

Question 71

Congenital Cataracts

Answer 71

• clouding of the lens of the eye
• part of many birth defects
• Most important:
  
  • non-dysjunctions
    
    • Down syndrome (trisomy 21)
    • Trisomy 13

Question 72

Strabismus genetics

Answer 72

• autosomal dominant and autosomal recessive inheritance

Question 73

Iritis

Answer 73

most common form of uveitis

• inflammation of the iris
• s/sxs: ciliary flush, miosis, photophobia, and severe throbbing pain
  
  • unilateral, blurred or decreased vision
• tx: topical steroid drops

Question 74

Posterior Uveitis

Answer 74

uvea = choroid, ciliary body + iris

• s/sxs: blurred or decreased vision due to problems with blood flow (in the choroid), unilateral
• tx: systemic glucocorticoids

Question 75

Episcleritis

Answer 75

inflammation of the episclera

• s/sxs: distinguished from scleritis by lack of severe pain & lack of photophobia
  
  • mild irritation of the palpebral conjuctiva
• diagnosis: slit lamp exam, blanching with phenylephrine
• tx: supportive care
  
  • systemic NSAIDs
    *

Question 76

Scleritis

Answer 76

inflammation that involves the sclera and deep episclera

• women age 30-50 with connective tissue disease
• s/sxs:deep, boring ache, photophobia, unilateral, focal or diffuse eye redness
  
  • can have nodular or necrotizing
• diagnosis: clinical with slit lamp
• tx: systemic corticosteroids and/or systemic immunosuppresive therapy (consult rheum AND ophtho)

Question 77

Keratitis

Answer 77

inflammation of the cornea

• if bacterial:
  
  • staph, pseudomonas
• risk factors: Bells palsy (dry eye surfaces) and improper contact lens use
• s/sxs: sudden pain in the eye, redness, reduced vision, photophobia, ciliary injection, hazy cornea, conjunctival erythema
• diagnosis:
  
  • clinical, slit lamp, fluorescein
• tx: topical fluoroquinolones (moxifloxacin)
  
  • DO NOT PATCH
    *

Question 78

Endophthalmitis

Answer 78

infection/inflammation of the inner eye

• usually caused by staph epidermidis or staph aureus
  
  • usually after surgery or penetrating ocular trauma
• s/sxs: intense conjunctival hyperemia, loss of red light reflex, eyelid edema, hypopyon, ocular pain, vision loss
• tx:
  
  • intravitreal abx, maybe add IV abx

Question 79

Astigmatism

Answer 79

variable curvature of the cornea or lense → difficult to focus light

• s/sxs: headache, eyestrain, distorted or blurred vision at any distance
• tx: cylindrical lense to correct shape

Question 80

Myopia

Answer 80

“nearsightedness”

• point of focus is in front of retina b/c eye is too long or lense is too curved
  
  • can see near objects but not far objects
• dx: visual acuity testing
• tx: concave lense

Question 81

Hyperopia

Answer 81

“farsightedness”

• point of focus is behind the retina b/c the eyeball is too short or the lense is too flat
  
  • can see distant objects but not near ones
• dx: visual acuity testing
• tx: convex lens

Question 82

Strabismus

Answer 82

misalignment of one or both eyes

• stable ocular alignment not usually reached until ag 2-3mo, still persisting at 4-6 months? refer
• types: hypertropia (upward), hypotropia (downward), esotropia (inward), exotropia (outward)
• dx: cover-uncover test
• tx: patch the normal eye, eyeglasses, corrective surgery if severe

Question 83

acute narrow angle-closure glaucoma

Answer 83

increase IOP leading to damage of the optic nerve (emergency)

• risk factors: hyperopia, >60yo, asian, hyperopia, females, narrow angle or large lens
• s/sxs: sudden onset of severe ocular pain, unilateral, halos around lights and tunnel vision (loss of peripheral vision)
  
  • N/V, HA
• dx: tonometry (IOP>21mmHg), optic disc blurring
• tx: combination of topical agents (timolol, apraclonidine, pilocarpine) + systemic agents (PO/IV acetazolamide or IV mannitol)
  
  • topical beta blockers
  • alpha 2 agonists (aproacloonidine, brimonidine)
  • miotics/cholinergics (pilocarpine, carbachol)
  • prostaglandins (latanoprost)
• definitive tx: iridotomy

Question 84

Chronic open angle glaucoma

Answer 84

• slow, progressive painless, bilateral peripheral vision loss
• risk factors: AFrican American, >40yo, family history, DM
• s/sxs: usually asymptomatic until late into onset
  
  • tunnel vision progressing to central vision loss
  • physical exam: cupping of optic disc (increased cup to disc ratio) [larger cup inside the disc]
• tx: prostaglandin analogs (1st line) latanoprost cause ciliary muscle to relax and increased aqueous humor flow,
  
  • beta blockers (timolol), reduces aqueous humor production
• alpha 2 agonists (brimonidine, apraclonidine), reduces aqueous secretion
  
  • carbonic anhydrase inhibitor (acetazolamide)
  • laser therapy
  • surgery = last line

Question 85

Amblyopia

Answer 85

decreased visual acuity of one eye due to disuse during visual development

• **needs to be treated before age 8 if you want to avoid SEVERE vision loss**
• risk factors: strabismus, refractive errors (astigmatism, myopia, hyperopia), congenital cataract
• s/sxs: decreased visual acuity
• diagnosis: early screening
• tx: eyeglasses, patch the normal eye, cataract removal, tx of strabismus, atropine drops

Question 86

Amaurosis Fugax

Answer 86

transient monocular vision loss that lasts minutes and spontaneously recovers

• usually a retinal ischemia or emboli, TIAs, giant cell arteritis, migraine, lupus
• risk factors: DM, heart disease, smoking, HTN, hyperlipidemia, age, cocain use
• s/sxs: vision loss that descends over the visual field (often described as a curtain or shade) that usually resolves within the hour
• dx: clinical diagnosis
• tx: tx the underlying vascular issue

Question 87

Central Retinal Vein Occlusion

Answer 87

• risk factors: associated with Afib and carotid disease
  
  • HTN, advancing age, glaucoma, DM
• s/sxs: sudden onset, severe, painless unilateral vision loss
  
  • blood and thunder of the retina
• dx: fundoscopy
• tx: globe massagem, refer to optho/ED
  
  • decrease IOP
  • tx HTN!

Question 88

Central Retinal Artery Occlusion

Answer 88

• risk factors: associated with Afib and carotid disease
  
  • HTN, advancing age, glaucoma, DM
• s/sxs: sudden onset, severe, painless unilateral vision loss
  
  • cherry red spot on pale macula
• dx: fundoscopy
• tx: globe massagem, refer to optho/ED
  
  • decrease IOP
  • tx HTN!

Question 89

Vitreous Detachment

Answer 89

• can be associated with trauma
  
  • hemorrhage in pts with DM
• s/sxs: complaints of mild vision loss, floaters, cobwebs or flashes of light
• refer to optho

Question 90

Answer 90

Hyphema

blood in the anterior chamber of the eye

• referral, eye shield

Question 91

Answer 91

Hypopyon

collection of neutrophils and fibrin in the anterior chamber of the eye

• often associated with endophthalmitis
• referall to surgery and intravitreal abx

Question 92

Globe Rupture

Answer 92

ophthalmologic emergency

• significant visual acuity impairment, diplopia
• dx: r/o intraocular foreign body, check visual acuity
  
  • DO NOT TOUCH EYE
• tx: ABCs, and stabilization
  
  • apply rigid shield cup, keep head elevated at 30-40 degrees (do NOT want to increase IOP)
  • CT orbits if stable
  • immediate surgical referral

Question 93

Blowout Fracture

Answer 93

fracture of the inferior floor of the orbit

• “trap door” or “white-eye fracture” in children = elastic bones can snap shut on muscle or other tissue
• s/sxs: decreased visual acuity, diplopia, eyelid edema
• dx: CT scan = teardrop sign (herniation of the orbital fat inferiorly
• tx: nasal decongestant, avoid blowing nose or sneezing, corticosteroids
  
  • abx: ampicillin-sulbactam, or clindamycin
  • surgery if severe

Question 94

Diabetic Retinopathy

Answer 94

gradual, bilateral, painless vision loss

• most common cause of new, permanent vision loss in 20-74yos

can have non-proliferative: microaneurysms, cotton wool spots, hard exudates, blot and dot hemorrhages

or

proliferative retinopathy: neovascularization, and maculoedema

• dx: fundoscopy, vital signs
• tx: non-proliferative = glucose control, laser treatment
  
  • proliferative = VEGF inhibitors (bevacizumab), laser photocoagulation, treatment, glucose control

Question 95

Hypertensive Retinopathy

Answer 95

• associated with malignant HTN (uncontrolled high blood pressure)
• can be associated with non-proliferative retinopathy: microaneurisms, cotton wool spots, hard exudates, drussen bodies, flame hemorrhages
• or proliferative retinopathy: neovascularization + maculoedema
• dx: fundoscopy + vital signs
• tx: tx the HTN!!
  
  • non-proliferative: laser treatment
  • proliferative: VEGF inhibitors (bevacizumab), laser photocoagulation

Question 96

Retinal Detachment

Answer 96

When retina separates from the choroid

• risks: myopia, previous cataract surgery, advancing age, trauma
• s/sxs: sudden onset, unilateral,, **flashes of light**, floaters, spreading cutrain of darkness
• dx: fundoscopy or ocular u/s
• tx: keep pt supine with head turned toward side of detachment
  
  • emergent referal to retinal specialist to seal the defect
    *

Question 97

Macular Degeration

Answer 97

most common cause of permanent legal blindness in adults >75yo

• dry (atrophic): most common type and progressive (spanning over decades)
• wet (neovascular or exudative): occurs more rapidly and is more severe
• s/sxs: bilateral progressive central vision loss,
  
  • ​central scotoma, metamorphopsia (straight line appears bent)
• dx: dry = drusen bodies
  
  • wet = new, abnormal vessels that can cause hemorrhaging and scarring
  • fundoscopy, AMSLER GRID
• ​management of dry: zinc and vitamins C&E can slow progression
• tx of wet: intravitreal VEGF inhibitors (bevacuzimab, ranicuzimab) = decrease new and abnormal vessel growth
  
  • laser photocoagulation

Question 98

Orbital Cellulitis

Answer 98

• preseptal orbital cellulitis = outside of the orbit
• postseptal orbital cellulitis = inside the orbit (especially from sinus infection from the ethmoid sinus
• s/sxs:
  
  • preseptal and postseptal = tenderness, edema, erythema, discoloration of eyelid and fever
  • postseptal = decreased ocular mobility, pain with eye movement, proptosis, and decreased visual acuity
• dx: clinical, high resolution CT scan
• tx: admission + IV abx
  
  • vancomycin + ceftriaxone or cefotaxime (3rd gen)
• preseptal = outpatient if older than 1 year oral clindamycin (to cover MRSA)

Question 99

Optic Neuritis

Answer 99

inflammation of the optic nerve often due to acute inflammatory demyelination of the optic nerve

• associated with women 20-40yo, multiple sclerosis, and ethambutol
• s/sxs: unilateral, painful vision loss
  
  • decrease in color vision, central scotoma over hours to a few days, ocular pain worse with movement
  • 1/3 of pts have papillitis ( optic disc swelling)
• dx: clinical, MRI orbit, brain and spinal cord
  
  • swinging flashlight test
• tx: IV corticosteroids (methylprednisone) followed by PO corticosteroids
  
  • neuro and optho referral

Question 100

ptosis

Answer 100

drooping of eyelid

can be associated with CN III deficit or levator palpebrae muscle

referral to optho

Question 101

Proptosis

Answer 101

• aka exopthosis, protrusion of the eyeball
• **most common in adults with Graves Disease (hyperthyroid)
  
  • **most common in children with orbital cellulitis**
• s/sxs: red flags = eyepain/redness, HA, loss of vision, diplopia, fever, pulsating or neonatal
• dx:
  
  • acute unilateral = infection or vascular disorder
  • chronic unilateral = tumor
  • CT, MRI
  • order thyroid function testing
• tx: lubricate the cornea, systemic corticosteroid to reduce edema
  
  • may need surgery

Question 102

Hordeolum

Answer 102

aka stye = abscess of the meibomian gland, gland of Moll, or Gland of Zeiss)

• staph aureus
• s/sxs: pain, warm, erythematous, nodule or pustule on eyelid
• diagnosis: clinical
• tx: warm compresses, can use oral abx if accompanied by preseptal orbital cellulitis (dicloxacillin or erythromycin)
  
  • can add topical abx if actively draining (erythromycin or bacitracin)

Question 103

Answer 103

Entropion

inversion of the eyelid

• usually associated with advancing age, but can also be postinfection, trauma, or blepharospasm
• s/sxs: foreign body sensation, tearing, red eye
• diagnosis is clinical
• tx: surgery = refer to optho

Question 104

Answer 104

Ectropion

• eversion of the lower eyelid
• caused by advancing age, relaxation of tissue, cranial nerve VII palsy, and post-traumatic/surgical changes
• s/sxs: tearing (because puncta are no longer in contact with the eye) dry eye
• diagnosis is clinical
• tx: lubrication eye drops at night
  
  • tear supplements
  • definitive tx = surgery, refer to optho

Question 105

Chalazion

Answer 105

non-infectious blockage of internal Meibomian sebaceous gland, or zeiss gland

• often associated with acne rosacea
• s/sxs: non-tender localized eyelid swelling on the conjunctival surface of the eyelid
  
  • often larger, firmer, slower growing, and less painful than hordeolum
• diagnosis is clinical
• tx: warm compresses, abx eye drops
  
  • referral to optho for injection of glucocorticoid or incision + curettage if does not resolve

Question 106

Blepharitis

Answer 106

infection of the eyelids

• acute ulcerative: staph or HSV
• acute non-ulcerative: allergic
• chronic: meibomian gland dysfunction or seborrheic dermatitis
• s/sxs: pruritus or burning of eyelid margin, conjunctival irritation and tearing, photosensitivity, sensation of foreign body
• dx: slit lamp
• tx: supportive
  
  • warm compresses, cleansing of eyelid, keratoconjuctivitis sicca tx PRN
  • can use abx for acute ulcerative and chronic or topical corticostosteroid of nonulcerative

Question 107

Dacrocystitis

Answer 107

infection of the lacrimal sac

• often caused by staph aureus and strep
• s/sxs: pain, erythema, edema around lacrimal sac
  
  • pressure on lacrimal sac may exude mucoid or purulent material through the puncta
• diagnosis is clinical
• tx: mild = warm compresses and 1st gen ceph, or penicillinase-resistant penicillin (PO)
  
  • IV abx
  • not responding to tx? consider MRSA

Question 108

Corneal Abrasion tx

Answer 108

abx ointment (aminoglycoside tobramycin, gentamicin), or erythromycin and pupillary dilation

plus the tetanus immunization!!!

Question 109

pterygium

Answer 109

benign growth of the conjunctiva that results from chronic actinic irritation

• more common in sunny, dry, hot climates
• s/sxs: fleshy, trianngular growth of the bulbar conjunctiva that can spread across the cornea and induce astigmatism/affect vision
  
  • pinguecula doe NOT affect the cornea
• diagnosis is clinical
• tx: arifical tears or short course of topical corticosteroids, reassurance
  
  • referral if starting to affect vision for surgery

Question 110

Ocular Herpes

Answer 110

corneal infection with HSV

• s/sxs: ocular pain, foreign body sensation, photophobia, blurred vision, watery discharge
  
  • dendritic lesions with fluorescein stain
• dx: dendritic ulcer or viral cx
• tx: topical ganciclovir or trifluride OR PO acyclovir or valacyclovir

Question 111

Cataract

Answer 111

thickened lens associated with aging, smoking, DM, long-term steroid use, trauma, congenital, and children exposed to too much O2

**leading cause of reversible blindness**

• s/sxs: cloudy/blurry vision, glare in vision (especially at night), halos, perception of faded color, yellowing/browning of vision
  
  • NOT PAINFUL
  • absent red light reflex, opaque lens
    
    • cortical spokes, or posterior subcapsular
• dx: slit lamp exam
• tx: surgery

Question 112

Subconjuctival Hemorrhage

Answer 112

usually result of minor local trauma, straining, sneezing, or coughing

• diagnosis is clinical
• tx: reassurance = should resolve within 2 weeks

Question 113

What is the medical term for asymmetric pupils?

Answer 113

Anisocoria

Question 114

Anatomy of the Tympanic Membrane

Answer 114

Question 115

Semicircular canals

Answer 115

• filled with endolymph
• respond to rotation of the head in 3 planes
• hair cells at the base of the semicircular canals are distorted when the head moves in the x, y, z planes

Question 116

Vestibule

Answer 116

• made up utricle and saccule
• hair cells within the vestibule are pressed down by gravity, or if gravity /accelearation changes → hair cells become distorted

Question 117

Vestibular pathway

Answer 117

• for balance and sensation of balance
• vestibular hair cells send signals via CN VIII (vestibulocochlear)
• received by pons and medulla oblongata → cerebellum and cerebral cortex

Question 118

Nystagmus

Answer 118

• rapid, involuntary eye movement as a result of activation of the vestibular system (usually side to side)

Question 119

Risk factors of otitis Media

Answer 119

smoking

family hx of OM

bottle feeding

attending daycare

Question 120

Bacteria associated with otitis externa and risk factors

Answer 120

• Bacterial:
  
  • Pseudomonas aerugonisa, Proteus vulgaris, staph aureus, or E. coli
• Fungal:
  
  • Aspergillus niger
  • Candida albicans
• Risk factors:
  
  • allergies
  • psoriasis
  • eczema
  • seborrheic dermatitis
  • decreased canal acidity (possibly due to repeated presence of water)
  • irritants (e.g. hair spray/dye)
  • **skin maceration that sets the stage for bacterial infection **

Question 121

Non-syndromic Hearing Loss

Answer 121

• partial or total hearing loss that not associated with other s/sxs
• classifications:
  
  • Autosomal Dominant (DFNA)
  • Autosomal Recessive (DFNB)
  • X-linked (DFNX)
  • each has subtypes number in the order they were discovered
• Mostly sensorineural but can less commonly be conductive
• Mixed inner and middle ear hearing loss. = DFNX2
  
  • called mixed hearing loss

Question 122

Syndromic Hearing Loss

Answer 122

• hearing loss in addition to other medical issues
• characterized by mode of inheritance:
  
  • autosomal recessive (AR)
  • autosomal dominant (AD), or x-linked
• 3 major syndromes:
  
  • Usher syndrome: retinitis pigmentosa and senorineural hearing loss
  • Pendred syndrome: abnormal iodine metabolism in addition to hearing loss
  • Jervell and Lange-Nielsen syndrome: profound sensorineural hearing loss, cardiac arrhythmias caused by prolonged QT interval

Question 123

Waardenurg Syndrome

Answer 123

• ***Most common form of autosomal dominant sensorineural hearing loss***
  
  • 3% of childhood hearing loss
  • bilateral or unilateral sensorineural hearing loss, pigment abnormalities, and defining features of the face
    
    • white hair in front, differently colored irises (heterochromia irides), graying early, and vitiligo
    • face features: widely spaced medial canthi, broad nasal root, and unibrow (synophrys)
• tx: cochlear implant

Question 124

Vestibular Schwannoma and Neurofibromatosis 2

Answer 124

• benign tumors of the vestibularcochlear nerve (CNVIII)
• NF2 = changes in the NF2 gene
  
  • regulations proteins production that functions as a tumor suppressor
  • usually caused by spontaneous mutation of the NF2 gene
    
    • otherwise inherited via autosomal dominant
• S/Sxs:
  
  • problems with balance, tinnitys and gradual hearing loss
  • people with NF2 have less cafe-au-lait spots on the skin than those who have NF1
• Tx: surgical removal if possible
  
  • radiation therapy
  • VEGF inhibitor bevacizumab (VERY EXPENSIVE)

Question 125

Environmental Impacts on Hearing

Answer 125

• noise
• aging
  
  • presbycusis
• ototoxic drugs
  
  • aminoglycosides
    
    • can synergistically act with noise to cause severe hearing problems
• viral and bacterial infections
  
  • Rubella (less so with vaccine and rhogam)
  • Cytomegalovirus is most common cause of congenital deafness*****
• diet, stress, drugs, certain diseases and life styles

Question 126

3 Major Syndromes associated with Autosomal Recessive inheritance of hearing loss

Answer 126

• Usher Syndrome:
  
  • retinitis pigmentosa and sensorineural hearing loss
• Pendred Syndrome:
  
  • abnormal iodine metablism with hearing loss
• Jervell and Lange-Nielsen Syndrome:
  
  • profound hearing loss
  • cardiac arrhythmias caused by prolonged QT intervals

Question 127

Waardenburg Syndrome

Answer 127

• Autosomal dominant sensorineural hearing loss
• white forelock, heterochromia, premature graying, vitiligo
• unilateral sensorineural hearing loss
• tx: cochlear implant

Question 128

Neurofibramatosis 2

Answer 128

• noncancerous tumors of the nerves vestibular cochlear nerves
  
  • bilateral acoustic neuromas/vestibular schwannomas
• mutation of the NF2 gene → tumor suppresor gene
• less cafe au lait spots than in NF1
• Autosomal Dominant
• gradual hearing loss, tinnitus, balance problems

Question 129

With the advent of vaccines what is the most common cause of congential deafness

Answer 129

• cytomegalovirus

Question 130

Nasal Cavity: type of mucosa, and bones

Answer 130

nasal septum divides the nasal cavity (has anterior cartilage portion and posterior bony portion (perpendicular plate of the ethmoid bone, vomer, nasal conchae)

Question 131

Location of Nosebleeds and Structures Involved

Answer 131

• Anterior: Kiesselbach’s plexus (4 arteries anastomose here)
• Posterior: Woodruff plexus (sphenopalatine artery)

Question 132

Acute vs Subacute vs. Chronic (Rhino)sinusitis

Answer 132

• acute = < 4 weeks
• subacute = >4 weeks but < 3 months
• chronic = >3months (12 weeks)

Question 133

Chronic Bacterial Rhinosinusitis

Answer 133

• lasts longer than 12 weeks/3 months ***
• common bacteria: pseudomonas, klebsiella pneumonia, enterobacter spp. e.coli, and S. aureus
• 4 cardinal signs:
  
  1. mucopurulent drainage of the anterior or posterior portion of the nose
  2. nasal obstruction/ congestion/blockage
  3. facial/sinus pain, pressure, or fullness
  4. loss of sense of smell or reduced sense of smell (anosmia or hyposmia )
• tx: single agent: Augmentin
  
  • double agent:
    
    • metronidazole plus cefdinir or bactrim

1. CRS with nasal polyposis (with nasal polyps)
2. Allergic fungal rhinosinusitis (more common in DM patients)
3. CRS without nasal polyposis (without nasal polyps)

Question 134

What medication is contraindicated in an asthmatic patient with nasal polyps?

Answer 134

ASA - aspirin

Question 135

Stress Incontinence Tx

Answer 135

• kegel exercises: 3-6 weeks of daily exercises, 200/day
• vaginal estrogens
• pessary
  
  • SEs: vaginal irritation, foul-smelling discharge, UTIs
• surgery → mid-urethral sling
• weight loss

Question 136

Prostate Cancer Etiology, S/sxs, PE, Dx, Tx

Answer 136

• most are adenocarcinomas
• associated with the BRCA1 gene
• Risk factors: african american, old age, family hx
• S/sxs: urinary retention (more likely sign of BPH), decrease in urine stream strength
  
  • back pain (metastatic disease)
  • painful ejaculation
• PE: DRE: hard, nodular, enlarged, and asymmetrical prostate
• Dx:
  
  • indications for transrectal biopsy with normal rectal exam → PSA > 10 or abnormal transrectal U/S
  • PSA > 4: U/s with needle biopsy
  • PSA >10: bone scan to r/o metastases
• Tx;
  
  • radical prostatectomy → complication = erectile dysfunction & urinary incontinence
  • with metastases: need androgen deprivation therapy (leuprolide) → type of medical castration, but can be reversible
    *

Question 137

Calcium Nephrolithiasis Risk factors and Prevention

Answer 137

• calcium oxalate = most common
• Radiopaque
• Risk factors: decreased fluid intake, high urinary calcium or pH, high animal protein intake, hypercalcemia, males, medications (loop diuretics, acetazolamide, antacids)
• Prevention: increased fluid intake, thiazide diuretics, citrate, low sodium diet, decreased animal protein diet

Question 138

When to screen for PSA

Answer 138

DISCUSS WITH PATIENT

• men age 55-69 yo
• 50 years old if first degree family hx
• 45-50 if african american

Question 139

BPH S/sxs, PE, Dx, & Tx

Answer 139

Benign Prostatic Hyperplasia

• 50% of men have BPH by age 60, >90% by age 85
• S/sxs: difficulty starting stream, post-void dribbling, hesitancy (start and stop)
  
  • nocturia
  • weak urinary stream
• PE: digital rectal exam → uniformly enlarged firm and rubber prostate
• Dx:
  
  • DRE +PSA
  • PSA < 4 = normal
  • PSA > 4 → BPH, prostate cancer, prostatitis
  • UA to r/o other causes
• Tx:
  
  • if mild → watchful waiting
  • alpha blockers can provide the most rapid relief (smooth muscle relaxation of porstate and bladder neck
    
    • tamsulosin, prazosin, terazosin (shrink size of prostate)
      
      • finasteride & dutasteride -> 5-alpha reductase inhibitors that block the conversion of testosterone to DHT, increased levels of testosterone causes shrinking of prostate and increased hair growth
  • TURP (transurethral resection of the prostate) if unresponsive to meds
  • 5-alpha reductase inhibitors

Question 140

UTI prevention

Answer 140

• drink adequate amount of water
• avoid delay in voiding
• personal hygiene
• cranberry juice/tablets
• abx prophylaxis for 3 UTIs/12 months
  
  • Bactrim/Cipro

Question 141

Major Risk Factors of Coronary Artery Disease (CAD)

Answer 141

• Diabetes Mellitus (Worst risk factor, considered a CAD equivalent)
• Smoking (Most important modifiable risk factor)
• Hyperlipidemia, HTN
• Men >45yo, Women >55yo
• Fam Hx of CAD: (first degree relative – father or brother before age 55, mother or sister before age 65)

Question 142

Post MI Complications

Answer 142

• Pericarditis: 1-3 weeks post MI (Dressler Syndrome)
• VSD (ventricular septal defect: 1-5 days post MI: shock, new murmur, pulmonary edema
• Acute Mitral Regurg: shock, apical murmur, pulmonary edema
• new or recurrent MI: chest pain, new ECG changes possible, new bump in troponins

Question 143

Acute vs. Chronic Heart Failure

Answer 143

• S/sxs:
  
  • Chronic Heart Failure (compensated):
    
    • congestion
    • laterally displaced apical impulse
  • Acute Heart Failure:
    
    • breathlessness
    • rapid weight gain
    • fluid build-up in the lungs and around the body
    • inadequate time for compensation: largely systolic (HTN crisis, acute MI, papillary muscle rupture); often fatal

Question 144

Systolic Heart Failure

Answer 144

• Definition: heart failure with decreased ejection fraction
  
  • impaired contractility
  • thin ventricular walls (DILATED)
  • S3 gallop (sys-tol-ic)
• Etiology:
  
  • ischemic heart disease, rapid HTN, dilated cardiomyopathy (LEADING CAUSE), myocarditis, congenital, post-surgical, PE, sepsis

Question 145

Diastolic Heart Failure

Answer 145

• Definition: Heart failure with preserved ejection fraction
  
  • impaired filling/relaxation
  • thick ventricular walls (**Hypertrophied**)
  • S4 gallop (Di-a-stol-ic)
• Etiology:
  
  • HTN, aortic stenosis, restrictive & hypertrophic cardiomyopathy, fibrosis, amyloidosis, sarcoidosis, constrictive pericarditis, normal aging, CAD scarring

Question 146

Tx of Heart Failure

Answer 146

• **initial management usually consists of an ACEI & (maybe a beta blocker) + diuretic (for sxs)**
• Long Term Tx (Afterload reduction:
  
  • ACE Inhibitors (Captopril, Enalapril, Lisinopril): reduce afterload by vasodilation & BP reduction, useful in pts with EF <35%,mainstay of tx, (adverse effects: hyperkalemia, cough, angioedema, & elevated creatinine)
  • Angiotensin II Receptor Blockers (Losartan, Valsartan): blocks effects of angiotensin II, indicated in pts who cannot tolerate ACEI (cough)
  • Angiotensin Receptor Neprilysin Inhibitor (Sacubitril/Valsartan): inhibits breakdown of BNP so BNP no longer becomes a reliable marker in pts taking this
  • Beta-Blockers (Carvedilol, Metoprolol, Bisprolol): usually added after ACEI or AR
• Long Term Tx (Preload Reduction)
  
  • Loop Diuretics (furosemide, bumetanide, torsemide): inhibit water transport across the Loop of Henle, effective for sx tx.
  • potassium sparing diuretics (spironolactone, eplerenone): aldosterone antagonist, decreased mortality
  • Thiazides (hydrochlorothiazide, Metolazone): inhibits DCT reabsorption of Na+
• Long Term Tx (Positive Inotropes):
  
  • Digoxin: positive inotrope; 2nd line for pts in CHF with sinus rhythm, 1st line for pts with afib + CHF

Question 147

Primary Prevention of ASCVD in Age 40-75 and LDL-C ≥ 70 to <190 mg/dL without diabetes mellitus

Answer 147

10-year ASCVD risk percent begins risk discussion:

• <5%: “low risk”
  
  • emphasize lifestyle to reduce risk factors
• 5-<7.5%: “borderline risk”:
  
  • If risk enhancers present then risk discussion regarding moderate-intensity statin therapy
• ≥7.5-<20%: “Intermediate Risk”
  
  • Risk discussion:
    
    • if risk estimate + risk enhancers favor statin, initiate moderate-intensity statin to reduce LDL-C by 30-49%
    • if unsure, can use CAC score
• ≥ 20%: “high risk”:
  
  • initiate statin to reduce LDL-C ≥ 50%

Question 148

At what LDL-C level do you initiate high intensity statin with no risk assessment?

Answer 148

LDL-C ≥ 190 mg/dL

Question 149

Best meds to lower elevated LDL

Answer 149

• Statins (Rosuvastatin, atorvastatin, etc) → inhibit HMG Co-A reductase
  
  • impair production of cholesterol in the liver → upregulation of LDL receptors
• Bile Acid Sequestrants (Cholestyramine, colesevelam, colestipol) & Cholesterol absorption inhibitors (Ezetimibe)
  
  • impair enterohepatic recirculation and gut absorption → less hepatic cholesterol → upregulation of LDL receptors

Question 150

Best Meds to Lower Triglycerides

Answer 150

• Fibrates (fenofibrate, gemfibrozil): inhibit triglyceride synthesis = Drug of Choice;gemfibrozil should NOT be given with statins
• Niacin

Question 151

Best Meds to Increase HDL

Answer 151

• Niacin
• Fibrates (fenofibrate, gemfibrozil): inhibit triglyceride synthesis = Drug of Choice;gemfibrozil should NOT be given with statins

Question 152

Abnormal Lipid Values

Answer 152

• Low HDL <40 mg/dL
• High LDL > 190 mg/dL
  
  • high LDL in diabetic >70 mg/dL
• high total cholesterol >250 mg/dL
• high fasting triglyceride >150 mg/dL

Question 153

Secondary HTN Definition and Causes

Answer 153

• Definition: SBP ≥130 and/or DBP ≥80 WITH identifiable cause
• Causes:
  
  • Primary aldosteronism = MOST COMMON -> increases sodium and water retention in kidneys and potassium excretion
  • renal vascular disease
  • pheochromocytoma
    
    • adrenal tumor that secretes catecholamines (ie norepi and epi)
  • Cushing’s Syndrome
    
    • activation of the renin-angiotensin system
  • Congenital Adrenal Hyperplasia
  • Hyperthyroidism
  • Myxedema
    
    • associated with hypothyroidism
  • Coarctation of the Aorta
  • Excessive alcohol intake
  • Use of Oral Contraceptives

Question 154

Secondary HTN Red Flags, Dx, & Tx

Answer 154

• Red Flags:
  
  • HTN at an early age <25 without a family hx
  • HTN first develops >50 yo
  • previously controlled now refractor
  • Pt is refractory on antihypertensive medications or has severe BP
• Dx:
  
  • when HTN is newly diagnosed consider ordering:
    
    • urinalysis
    • spot urine albumin: creatinine ratio → albuminuria ratio = >30mg/day
      
      • indicative of CKD
    • Blood tests
      
      • creatinine, K, Na, fasting glucose = BMP
      • lipid panel
      • TSH
    • EKG
• Tx:
  
  • tx the underlying condition and aim for BP <130/80

Question 155

Acute Bacterial Endocarditis Definition and organism

Answer 155

• Definition: infection of a normal valve with a virulent organism (usually S. Aureus).
• Rapidly destructive (fatal < 6 weeks if untreated)

Question 156

Beck’s Triad

Answer 156

Associated with Cardiac Tamponade

1. elevated JVP
2. muffled heart sounds
3. systemic hypotension

Question 157

Mnemonic to Remember Medical Tx of STEMI

Answer 157

MOAN & BASH

Morphine, oxygen if O2 <90%, Aspirin 162 mg, Nitro q 5 min (don’t give to pts with systolic <90, or to inferior MI with R ventricular involvement → dependent on preload and nitro decreases preload)

Beta blockers (Decrease remodeling, decrease oxygen demand of heart, decreases HR, improve L ventricular hemodynamic funx, reduce incidence of ventricular arrhythmias; Contraindication in Heart block, high risk for cardiogenic shock) , ACE-I/ARB (more for long term use → improve L ventricular EF, mortality rate), Statin, Heparin (antithrombotic therapy → impede progression of thrombus in coronary artery)

TPA if pt cannot have reperfusion from cath lab in <90minutes from door to lab

Question 158

Dressler’s Syndrome

Answer 158

Post-MI pericarditis

tx = aspirin or colchicine

Question 159

Triad of R Ventricular Infarction

Answer 159

1. JVD
2. Clear Lungs
3. Positive Kussmaul Sign
   
   1. paradoxical rise of JVP with inspiration (blood backs up into vein during inspiration due to failure of R ventricle)

Question 160

3 populations with atypical sxs for acute MI

Answer 160

elderly, women, diabetics

Question 161

Answer 161

Heliotrope Sign (associated with Dermatomyositis**)

• ​dermatomyositis = autoimmune disease that leads to degeneration of the skin and muscle
  
  • characterized by muscle weakness heliotrope sign and Gottron’s Papules

Question 162

Answer 162

Gottron’s Papules (indicative of Dermatomyositis**)

• dermatomyositis = autoimmune disorder that leads to the degeneration of the skin and muscle
  
  • characterized by muscle weakness and Gottron’s papules and Heliotrope sign
• Gottron’s papules = over the joints of the hands

Question 163

Answer 163

Butterfly/Malar Rash

• indicative of Systemic Lupus Erythematosus
  
  • worsened when exposed to the sunlight
• systemic lupus erythematosus also will show a rash on the hands that spares the knuckles

Question 164

Net Effect of Increased PTH

Answer 164

hypercalcemia, hypophosphatemia
-PTH analogs: teriparatide 20 mcg SC QD-> stimulate osteoblast function, increases GI absorption of calcium, increases renal tubular resorption of calcium and increases strength of bones

Question 165

Causes of Pre-Renal Acute Renal Failure

Answer 165

• due to volume loss, heart failure, or loss of peripheral vascular resistance → all lead to loss of perfusion in kidneys
  
  • NSAIDs also can cause this (vasoconstriction of the afferent arteriole)
  • ACEI and ARB block effect of angiotensin (vasodilation of the efferent arteriole)
  • Diuretics
• ***Kidneys are working fine, the organs that perfuse the kidneys arent working properly***

Question 166

PreRenal Acute Renal Failure S/sxs, Dx, and Tx

Answer 166

• S/sx: weak oliguria (decreased urine output), dizziness, sunken eyes, tachycardia, orthostatic BP changes
• Dx: BUN:Cr > 20:1, urine osmolality > 500, FeNa <1%, FeUrea <35%, Urine Na <20 mEq/L
• Tx: tx with fluids, cardiac support, and/or tx shock

Question 167

PostRenal AKI Etiology, S/sxs, dx, tx

Answer 167

• Etiology: obstruction (most common = prostate), bilateral outlet obstruction or bilateral ureteral obstruction
• S/sxs: oliguria or anuria +/- suprapubic pain
• Dx: foley catheter placement to find source of obstruction
  
  • if large urine output after foley = bladder, urethra, BPH
  • if low urine output after foley = ureter obstruction or pathology
  • Renal U/S but CT is most specific!!
• tx: removal of obstruction → if done rapidly = quick reversal of AKI

Question 168

Acute Tubular Necrosis Etiology

Answer 168

• ***Type of Intrinsic AKI***
• Etiology = kidney ischemia or toxins
• prolonged pre-renal AKI = most common cause
• Major Causes:
  
  • drugs and toxins: ampho B, cisplatin, sulfa drug, aminoglycosides, radiocontrast media, NSAIDs, ACEI, cocaine use
  • ischemic related ATN : dehydration, shock, sepsis, hypotension
  • endogenous toxins: heme from hemolysis, myoglobin from rhabdomyolysis (iron is myoglobin is toxic to renal epithelial cells), tumor lysis syndrome, muscle breakdown in a marathon runner

Question 169

Acute Tubular Necrosis S/sxs, Dx, Tx

Answer 169

• S/sxs: Oliguria, increased SCr etc
• Dx: urinalysis = muddy brown casts (renal tubule epithelial cells), myoglobinuria, hemoglobinuria
  
  • FeNa >2%, FeUrea >35%, Urine Osmolality <350
• Tx: remove toxin or re-perfuse kidney via IV fluids
  
  • can use loop diuretics if pt is euvolemic and not urinating
  • ***most pts return to baseline within 7-21 days ***

Question 170

Etiology of Interstitial Nephritis

Answer 170

• Etiology: immune-related response
• due to:
  
  • drugs: PCN, sulfa (bactrim), NSAIDs, phenytoin, Diuretics, etc
  • immunologic & infx disease: strep (get an ASO antibody), SLE, CMV, Sjogren’s, sarcoidosis

Question 171

Interstitial Nephritis S/sxs, Dx, & Tx

Answer 171

• ***type of intrinsic AKI***
• S/sxs: oliguria (decreased urine output), increased SCr
• Dx: urinalysis = WBC cats, WBCs, and eosinophils
  
  • acute azotemia (accumulation of nitrogenous waste, BUN)
  • diagnosed with RENAL BIOPSY → interstitial inflammatory cell infiltrates
• Tx: d/c offending drug, corticosteroids, dialysis PRN
  
  • → usually self-limiting if caught early
  • most people recover kidney function within 1 year

Question 172

Etiology of Nephrotic Syndrome

Answer 172

• glomerular damage results in higher loss of proteins in the urine
• Most common primary causes:
  
  • membranous nephropathy: most common in non-DM adults associated with malignancy
  • MINIMAL CHANGE DISEASE: most common cause in children, idiopathic nephrotic syndrome sxs improve after tx
  • focal segmental glomerulosclerosis: obese pts, heroin, and HIV (+) black males
• Most common Secondary Cause:
  
  • lupus
  • DM

Question 173

Nephrotic Syndrome S/sxs, Dx, & Tx

Answer 173

• S/sxs: peripheral or periorbital edema, ascites, weight gain, fatigue, and HTN, frothy urine
• Dx: serologic testing and renal biopsy
  
  • proteinuria >3.5g/day = diagnostic ( 24h urine collection)
  • urinalysis: free lipid or oval fat bodies or fatty casts → lipiduria
  • Hypoalbuminemia < 3.5g/dL
  • hyperlipidemia LDL > 130mg/dL, Triglycerides > 150mg.dL
• Tx:
  
  • tx the causative disorder, corticosteroids

Question 174

Etiology of Glomerulonephritis

Answer 174

• inflammation of the glomeruli due to blockage from immune complexes → immune response causes this
• Post-Infectious Group A strep → diagnosed with ASO titers and low serum complement
• IgA Nephropathy (berger disease): Most common cause of acute glomerulonephritis
  
  • young males after URI or GI infx (within 24-48 hours) → IgA immune complexes are first line defense in respiratory/GI secretions so infx → overproduction which damages the kidneys
  • more common in asian population
• Membranoproliferative Glomerulonephritis: caused by SLE, viral hepatitis (Hep C)
  
  • secondary to immune-complex deposition or complement mediated mechanism

Question 175

Glomerulonephritis S/sxs, Dx, & Tx

Answer 175

• S/sxs: edema + HTN + hematuria + RBC casts, jaundice, HTN
• Dx: urinalysis = hematuria >3 RBCs/HPF + RBC casts + proteinuria (1-3.5g/day)
  
  • ASO titer for post-strep
  • serum complement = decreased (not always
  • RENAL BIOPSY = GOLD STANDARD
• Tx: steroids and immunosuppressive drugs to control inflammation due to immune response
  
  • dietary management = salt and fluid restrictions
  • Dialysis if symptomatic azotemia
  • ACEI/ARBs (enalapril or losartan) are renoprotective → BP goal <130/80
  • use meds to control hyperkalemia

Question 176

Definition of CKD

Answer 176

dx: GFR < 60mL/min/1.73m2 for 3 months or any of the following:

• albuminuria: urine albumin: creatinine ratio >30mg/day
• proteinuria: urine protein: creatinine ratio > 0.2
• hematuria
• structural renal abnormalities ( solitary kidney, hx of abnormal renal histology hx of renal transplant)

Question 177

Etiology of CKD

Answer 177

• Diabetes = MOST COMMON CAUSE (30%)
• HTN (25%)
• chronic glomerulonephritis (15%)
• interstitial nephritis, polycystic kidney disease, obstructive uropathy

Question 178

S/sxs of CKD

Answer 178

• Pruritus = common, but difficult to tx
• Cardio: HTN → caused by salt and water retention → decreased GFR = stimulation of RAAS → increased BP → CHF due to volume overload, HTN, anemia → pericarditis
• GI: (usually due to uremia) nausea, vomiting, loss of appetite
• Neuro: lethargy, confusion, tetany → (due to hypocalcemia), uremic seizures, peripheral neuropathy
• Heme: normocytic, normochromic anemia (secondary to deficiency of erythropoietin)
  
  • bleeding secondary to platelet dysfunction→ platelets do not degranulate in uremic environment
• Endo/Metabolic:
  
  • Ca²⁺/Phosphorus disturbances→ decreased renal secretion of phosphate leads to hyperphosphatemia → decreased production of 1,25-dihydroxy vitamin D → hypocalcemia → hyperparathyroidism
• hyperkalemia → decreased secretion and acidosis
• Fluid & Electrolyte problems:
  
  • volume overload: watch for pulm edema
  • hyperkalemia: due to decreased urinary secretion
  • hypermagnesemia: secondary to reduced urine secretion
  • hyperphosphatemia: decreased clearance of phosphate
  • metabolic acidosis: due to loss of renal mass (& therefore decreased ammonia production) & kidneys’ inability to secrete H⁺

Question 179

Tx of CKD

Answer 179

• Tx: ACEI and ARBs → slow progression of renal dysfunction
  
  • manage the comorbidities!! : control HTN, glycemic control (A1C 6.5-7.5%), cholestrol control, tobacco cessation
• Maintain HGB at 11-12 g/dl → Do not want to bring pt up to normal hgb levels → pro-thrombotic b/c it thickens the blood & increases mortality
• Dietary management: protein restriction, calcium and vitamin D supplements, limit water, sodium, and potassium and phosphorus
• Need for hemodialysis or kidney transplant
• PCV-23
• Fluid overload management: dietary salt <2 gm/day
• GFR > 30 → thiazide diuretics (hydrochlorothiazide, chlorthalidone)
• GFR <30 → loop diuretics (furosemide, torsemide, bumetanide)
• can use phosphorus binders to reduce hyperPTH → calcium carbonate, calcium acetate, sevelamer, lanthanum, iron
• tx the acidosis: may reduce risk of CKD progression → NaHCO3- → goal bicarb level >22

Question 180

NSAIDs and Sodium

Answer 180

NSAIDs reduce renal prostaglandins

and prostaglandins inhibit the action of ADH

so NSAID use can increase action of ADH and cause increased water reabsorption

Question 181

Desmopressin (DDVAP)

Answer 181

synthetic analogue of ADH

Act on V2-receptors at the collecting duct → reabsorption of water

used to tx central diabetes insipidus → the underlying pathophys behind isovolemic hypernatremia

also used to tx von Willebrand

Question 182

Hypokalemia Tx

Answer 182

When to tx? <3.5 mEq/L and/or pt is symptomatic

• treatment:
  
  • oral: K-chloride, KPO₄, K-acetate, K-citrate, k-gluconate
    
    • IV: if >10 mEq/L should be monitored via telemetry
  • other: diuretic induced (spironolactone- K+ sparing diuretic)
    
    • correct hypomagnesemia
      
      • ****low magnesium makes body resistant to K+ replacement, so tx mg deficiency first or concurrently*****
    • correct acid-base imbalance

Question 183

Goodpasture’s Syndrome

Answer 183

• causes rapidly progressive Glomerulonephritis (nephritic syndrome)
• anti-glomerular basement membrane
• presentation:
  
  • lungs/kidneys hemorrhage
  • teenagers & >50 years
  • rapidly progressive→ fatal
• Pathology:
  
  • antibodies against the glomerular basement membranne
    
    • often associated with crescent formation
• Tx:
  
  • cyclophosphamide + corticosteroids + plasmapheresis
    
    • due to high fatality → START RX while waiting for dx

Question 184

Hemolytic Uremic Syndrome

Answer 184

• Presentation:
  
  • E.coli O157:H7 (foodborne), Salmonella, etc. → undercooked meat consumption
  • bloody diarrhea that has resolved
  • fever; low platelets; AKI
• Dx:
  
  • often via serum assays
• Treatment: symptomatic manage,ent
  
  • HUS may require dialysis, 10% death rate

Question 185

Pauci-Immune Vasculitis S/sxs & Tx

Answer 185

• type of nephritic syndrome → cause of rapidly progressive glomerulonephritis
• Presentation: hematuria + signs of necrotizing small vessel vasculitis (diffuse skin lesion, lung hemorrhage, sinusitis, etc.)
• Tx: aggressive tx with steroids, cyclophosphamide or rituximab
• plasmapheresis → severe disease

Question 186

Lupus Nephritis S/sxs & Tx

Answer 186

• S/sxs: usually hx of lupus
  
  • SLE more common in female AA population
  • proteinuria, hematuria, + elevated creatinine
• Tx: dependent on biopsy classifications

Question 187

Dipstick positive for hemoglobin and myoglobin but no RBCs?

Answer 187

Rhabdomyolysis

Question 188

Normal Urine protein/creatinine ratio

Answer 188

< 0.2 or 200

aka SPOT urine protein/SPOT urine creatinine

Question 189

Normal Urine 24 hour protein

Answer 189

<200mg/day

Question 190

Microalbuminuria

Answer 190

30-300mg/g

Question 191

Macroalbuminuria

Answer 191

>300mg/g

Question 192

Rapidly Progressive Glomerulonephritis (RPGN)

Answer 192

when the “nephritis” is causing an AKI that is rapidly progressive over days to weeks
*causes:
*pauci immune GN: small vessel vasculitis
*Goodpasture syndrome: antibodies attack kidneys and lungs

• Nephritis:
  
  • RBC casts
  • proteinuria <3.5g

Question 193

Non-Oliguria vs Oliguria vs Anuria

Answer 193

Non-oliguria: >400mL/day

Oliguria: 100-400 mL/day

Anuria: <50mL/day

Question 194

Indications for Acute Dialysis

Answer 194

A: severe metabolic Acidosis

E: Electrolyte Problems (Hyperkalemia)

I: Intoxication (Antifreeze)

O: Overload of fluids

U:Uremic symptoms (pericarditis, altered mental status)

Question 195

At what GFR should we refer to nephrology?

Answer 195

GFR <30 ml/min/1.73m2 *CKD stage 4-5)

Question 196

Winter’s Formula

Answer 196

to calculate expected pCO₂

• Expected pCO₂ = (1.5 x bicarb) + 8 +/- 2
• if pCO_{2 = higher than expected → additional respiratory acidosis}
• if PCO_{2 = lower than expected → additional respiratory alkalosis}

Question 197

Albuminuria

Answer 197

urine albumin: creatinine ratio >30 mg/g (per day)

Question 198

Aldosterone

Answer 198

Made in the adrenal cortex

causes sodium and water retention in distal convoluted tubule

Causes K excretion in principal cells of renal Collecting Duct and K reabsorption in intercalated cells of CD

Question 199

ACEI/ARBs in CKD

Answer 199

1st line therapy for HTN in early CKD as they “tell kidneys to take a break & not filter so hard”

Will cause slight incr in SCr. Expected and ok as long as <30% and proteinuria is improving.

Watch K as ACEi/ARB can increase

Do not use ACEi & ARB together d/t incr risk of AKI, hyperkalemia, hypotension

Question 200

When are q-waves consider pathological?

Answer 200

• when they are 1 small box wide and at least 1/3 the height of the QRS complex
• this signifies a previous MI

Question 201

Primary Adrenal Insufficiency: General info, S/sxs, & PE

Answer 201

Aka Addison’s Disease

• Definition: Problem with the adrenal gland → lack of cortisol & aldosterone
  
  • MCC:autoimmune destruction and adrenal metastases
  • Worldwide: TB, secondary infx
• S/sxs:
  
  • hyperpigmentation: d/t increased POMC (proopiomelanocortin) → melanocytes
  • Salt craving b/c body is unable to retain salt
  • hypotension, fatigue
  • Myalgias
  • GI complaints, weight loss
    *

Question 202

Primary Adrenal Insufficiency: Dx & Tx

Answer 202

Aka Addison’s disease: Problem with the adrenal gland (the cortex)→ lack of cortisol & aldosterone

• Dx:
  
  • High dose cosyntropin (synthetic ACTH) stimulation test→ cortisol < 18 at 30 AND 60 minutes = PAI
  • 21-OH antibody: autoimmune
  • 17-OH-Progesterone: congenital adrenal hyperplasia
  • Low 8am cortisol (<5 miccrogram/dL), high ACTH (>2x UNL) and no increase in cortisol level after the ACTH stimulation test
  • High potassium
  • Low sodium
  • Glucose: low
• Tx:
  
  • *Will need life-long maintenance therapy*
  • Hydrocortisone PO daily 10-25mg AM, 5-10mg PM or prednisone 5 mg AM, 2.5mg PM
  • Medical Alert Bracelet/ necklace/road ID
  • Stress Dosing:
    
    • minor stress = 2-3x normal dose
    • severe stress = 5-6x normal dose
  • Stress Dose for Illness:
    
    • sick day rules for home (2-3x dose) & hospital
    • emergency injectable: for shock, significant blood loss

Question 203

Adrenal (Addisonian) Crisis

Answer 203

• Definition:
  
  • sudden worsening of symptoms in chronic adrenal insufficiency due to acute lack of cortisol precipitated by a stressful event
    
    • (infx, trauma, surgery, dehydration, salt deprivation, vomiting, diarrhea, sepsis)
• Pathophys:
  
  • normal response to stress = 3x increase in cortisol, but these patients are unable to increase cortisol to meet the demand
• S/sxs:
  
  • Hypotension, Shock & AMS
  • fever
  • Dehydration
  • N/v, anorexia
  • weakness, apathy
  • hypoglycemia, seizure
• Dx:
  
  • hyponatremia, hyperkalemia, hypoglycemia
  • *DO NOT delay tx while diagnostic testing is performed
• Tx:
  
  • Endocrine Emergency → will die if no tx
  • Emergent IV Isotonic Saline 100mL or 5% glucose in isotonic saline
  • Hydrocortisone 100mg IV then same dose q6h x 24 hours or continuous infusion → once stable 50 mg IV

Question 204

Secondary Adrenal Insufficiency

Answer 204

• Definition:
  
  • Insufficient pituitary ACTH (adrenocorticotropic hormone) production →Lack of cortisol
    
    • aldosterone intact due to renin angiotensin aldosterone system
• MCC: pituitary macroadenoma or a central nervous system tumor
  
  • can be identified on MRI and removed through transphenoidal resection
• S/sxs:
  
  • weakness, fatigue
  • anorexia, weightloss
  • salt craving
  • GI disturbance: N/V/D, abd pain
• Dx:
  
  • Low cortisol, low ACTH, and increase in cortisol after ACTH administration, but no aldosterone deficiency
  • No increase in ACTH after a CRH injection
  • Glucose: low
  • Sodium: low
  • Potassium = normal (no problem in adrenal gland so it can make aldosterone)

Question 205

Tertiary Adrenal Insufficiency

Answer 205

• Definition:
  
  • Insufficient CRH (corticotrophin-releasing hormone) production → decreased cortisol and normal aldosterone
  • MCC: sudden withdrawal of glucocorticoid therapy or after the cure of Cushing disease
• Dx:
  
  • Low cortisol, low ACTH, increase in cortisol after ACTH administration, but no aldosterone deficiency
  • ACTH levels increase after CRH injection

Question 206

Cushing Syndrome: etiology & s/sxs

Answer 206

• Etiology:
  
  • exogenous: high-dose glucocorticoid administration (MCC of hypercortisolism
  • endogenous:
    
    • Cushing’s Disease (85% of endogenous cases (Cushing syndrome symptoms produced by an ACTH-producing pituitary tumor)
    • ectopic ACTH-producing tumor, adrenal neoplasm, pituitary adenoma (corticotroph) → excess secretion of ACTH
• S/sxs;
  
  • HTN
  • Fat redistribution: truncal obesity, “moon face” round shaped face, buffalo hump, supraclavicular fat pad, thin extremities
  • Skin changes:
    
    • facial plethora (redness), thin skin, striae (purple or violaceous), easy bruising, acanthosis nigricans
  • Androgen excess: Hirsutism, oily skin, acne
  • psych disorders
  • cataracts

Question 207

Cushing Disease: Sx, Dx, & Tx

Answer 207

• S/sxs:
  
  • HTN
  • Fat redistribution: truncal obesity, “moon face” round shaped face, buffalo hump, supraclavicular fat pad, thin extremities
  • Skin changes:
    
    • facial plethora (redness), thin skin, striae (purple or violaceous), easy bruising, acanthosis nigricans
  • Androgen excess: Hirsutism, oily skin, acne
  • psych disorders
  • cataracts
• Dx:
  
  • ** loss of diurnal variation of cortisol (high throughout the day) → ideal to test at 12 am (low in normal pts) **
  • 24 hour urinary free cortisol (UFC)x2: not for CKD4-5
  • Overnight 1mg dexamethasone suppression test (DSP): measure an AM cortisol level with a dexamethasone level, positive if cortisol level > 1.8 (for cushing syndrome- ACTH independent b/c ACTH is suppressed by dexamethasone → NOT for cushing disease), not for patients taking OCP or estradiol
  • Late-Night Salivary Cortisol x2: not for night shift workers
  • *start with one of these exams & if abnormal, do another one
  • AM ACTH: determine if ACTH-dependent vs independent
  • AM DHEA-S: often low in hypercortisolism
• Tx:
  
  • Perform screening (see dx) and refer to endo
  • *tx depends on source:
    
    • pituitary: surgery, radiation, meds
    • adrenal: surgery, meds
    • ectopic: surgery, chemo

Question 208

Pheochromocytoma

Answer 208

• definition:
  
  • catecholamine secreting adrenal tumor which secretes norepi & epi autonomously and intermittently
  • 90% = benign, 10% = malignant
  • Associated with neurofibromatosis type 1, MEN 2A/2B, and Von Hippel-Lindau Disease
• etiology:
  
  • women = men, but women have more symptoms
• S/sxs:
  
  • Episodic: 5Ps →
    
    • 1.Pressure (HTN)
    • 2.Pain (headache)
    • 3.Perspiration
    • 4.Palpitations (tachycardia)
    • 5.Pallor
  • TRIAD: HA, diaphoresis, tachycardia
• Dx:
  
  • 24-hour catecholamines (in urine) including metabolites (metanephrine and vanillylmandelic acid)
  • MRI or CT of abdomen to visualize catecholamine secreting adrenal tumor
• Tx:
  
  • complete adrenalectomy
  • Preoperative non-selective alpha-blockade: phenoxybenzamine or phentolamine x 7-14 days followed by beta blockers to control HTN
  • ** Refer to Endo **
  • DO NOT initiate therapy with beta blockade to prevent unopposed alpha constriction during catecholamine release triggered by surgery, which could lead to life-threatening HTN

Question 209

When to consider Pheochromocytoma

Answer 209

• young pts with HTN
• family hx of pheochromocytoma
• radiologic incidentalomas
• shock after anesthesia, surgery, invasive procedure
• other: cardiomyopathy

Question 210

Hyperaldosteronism

Answer 210

• Primary:
  
  • etiology:
    
    • aldosterone-producing adenoma: 35%
    • bilateral idiopathic hyperplasia: 60%
    • unilateral idiopathic hyperplasia: 2%
  • Most common cause of endocrine HTN!!!!!!!!!!!! Prevalence: 5-10%
• Secondary:
  
  • Pathophys: increased renin → increased aldosterone via RAAS
  • etiology:
    
    • renal artery stenosis, renal artery hypoperfusion
• S/sxs:
  
  • HTN: HA or facial flushing
• When to consider testing for Primary Hyperaldosteronism:
  
  • HTN & hypokalemia
  • Resistant HTN (3+ drugs)
  • Adrenal incidentaloma + HTN
  • onset of HTN at young age <30
  • severe HTN (160/100)
  • any consideration of secondary HTN
• Dx of primary:
  
  • plasma aldosterone concentration (PAC): high (>15)
  • plasma renin activity (PRA): low (<1)
  • PAC-PRA ratio: > 20ng/dL
  • Potassium: usually normal, may be hypokalemic (but indicates very far along)
• Tx:
  
  • refer to endo for further testing & eval →
    
    • oral salt loading test or IV saline infusion test
      
      • if hyperaldosteronism is established then adrenal CT or MRI may be done
  • Spironolactone: blocks aldosterone from binding to mineralocorticoid receptors in the renal CD (increases aldosterone level since it is completing with spironolactone for the receptor, but lower BP since it blocks the effect of aldosterone)
  • Unilateral Adrenalectomy: if adrenal vein sampling lateralizes site of overproduction

Question 211

Process of Diagnosing an Adrenal Incidentaloma

Answer 211

1. CT imaging without intravenous contrast = best initial study
2. if adrenal mass is < 10 Hounsfield Units = dx of adrenal adenoma (lipid-rich adenoma)
   
   1. >40 HU = Malignant!
3. If adrenal mass is > 10 HU then do CT with IV contrast
   
   1. speed of & % washout of IV contrast from an adrenal nodule can be quantified
      
      1. benign lesions generally have > 50% washout of IV contrast
      2. adenomas washout IV contrast rapidly (<15min)
      3. Equivocal CT → MRI = next step

Question 212

Define Hirsutism

Answer 212

Excess body hair often due to excess androgens

seen in Cushing’s Disease

Question 213

Diabetes Insipidus (Central)

Answer 213

• Definition:
  
  • inability of the kidney to concentrate urine → production of large amounts of dilute urine caused by no production of AVP/ADH (produced by hypothalamus and stored with oxytocin in posterior pituitary) → water leaves collecting duct→ urine output increases
• Etiology:
  
  • idiopathic, destruction of posterior pituitary, head trauma, CNS tumor, infx
• S/sxs:
  
  • increased urinary frequency, polyuria, nocturia +/- enuresis, polydipsia
• PE:
  
  • normal, may show signs of dehydration
• Dx:
  
  • Urine output: increased (>40mL/kg/24hours)
  • Thirst: increased
  • Serum AVP: low (<1pg/mL)
  • Urine Osmolality: low (<300 mOsm/L)
  • Serum Sodium: high
  • Serum osmolality: high
  • Water deprivation Test: patient produces large amounts of dilute urine (even though they aren’t drinking water)
  • MRI:
    
    • evaluate posterior pituitary for “bright spot”(if absent → likely central DI) & pituitary stalk for trauma, hypophysitis, mass
• Tx:
  
  • assess pt’s ability to keep up with hydration
  • endocrine referral: for discussion of water deprivation testing and use of DDAVP

Question 214

Diabetes Insipidus (Nephrogenic)

Answer 214

• Definition:
  
  • inability of kidney to concentrate urine → production of large amounts of dilute urine due to partial or complete renal insensitivity to AVP at the level of the kidney
• Etiology:
  
  • congenital, pregnancy, meds (lithium, demeclocycline)
• S/sxs:
  
  • urinary frequency
  • polyuria, nocturia +/- enuresis, polydipsia
  • severe: neurologic sxs of hypernatremia: confusion, lethargy, seizures, coma
• PE:
  
  • normal (may show signs of dehydration: poor skin turgor, dry mucous membranes, drinking lots of water)
• Dx:
  
  • Urine Output: increased (>40 mL/kg/24 hours)
  • Thirst: increased
  • Serum AVP: high (>1pg/mL)
  • Urine Osmolality: low (<300 mosmol/L)
  • Serum Sodium: high
  • Serum Osmolality: high
  • **MRI has no role in dx
• Tx:
  
  • Thiazide diuretic (hydrochlorothiazide) &/or amiloride with low sodium diet
  • identify cause: d/c offending med if possible
  • Nephro consult
  • Pregnant: consult with OB before meds

Question 215

SiADH

Answer 215

• Definition:
  
  • excessive AVP/ADH production that impairs urinary water excretion & predisposes the pt to euvolemic hyponatremia if water intakes is not reduced
• Pathophys:
  
  • impaired urine dilution often caused by defect in osmotic suppression of AVP/ADH
• Etiology:
  
  • malignancy, brain trauma, stroke, subarachnoid hemorrhage, PNA, lung CA, meds
• S/sxs:
  
  • Severe: hyponatremia: confusion, lethargy, disorientation, seizures, coma
• PE:
  
  • normal
  • weight gain: increased in total body water by up to 10%
• Dx:
  
  • Urine Output: normal
  • Thirst: normal
  • Serum AVP/ADH: not measured
  • Urine Osmolality: high (>300 mOsmol/L)
  • Urine Sodium: high (>40 mEq/L)
  • Serum sodium: low (125-130)
  • Serum Osmolality: low
• Tx:
  
  • identify cause: d/x med if possible, look for malignancy & tx, look for lung (small cell lung cancer) or brain pathology & tx
  • free water restriction (<2 L/day)
  • endocrine or nephrology consult if no resolution: may need hypertonic (3%) NS infusion or tolvaptan/conivaptan (V2 agonists)

Question 216

Hyperkalemia and EKGs

Answer 216

• shortened QT
• ST depression
• Peaked T wave

Question 217

Treatment of Metabolic Acidosis

Answer 217

identify and tx underlying causes

• NaHCO₃^- indicated when:
  
  • renal dysfunction→ not enough HCO3- is regenerated
  • Severe acidemia: pG <7.10
  • goal: increase HCO3- by 10mEq/L; and ph> 7.2
  • ½ of the amount is given over 3-4 hours; then remainder given over 8-24 hours
  • ****1mEq/kg/dose and monitor***

Question 218

Tx of Metabolic Alkalosis

Answer 218

• pts rarely have symptoms due to alkalemia
  
  • sxs often related to volume depletion
    
    • muscle cramps
    • dizziness depending on position
    • HypoK+ → muscle weakness, polyuria, polydipsia
• Tx: tx the underlying cause
  
  • i.e. meds, citrate containing products (K-citrate used to tx metabolic acidosis), or acetate in parenteral nutrition → causes HCO3- levels to rise
  • alkalosis caused by vomiting, NG suction, or diarrhea +/- urinary Cl- (<25mEq/L) → saline infusion
  • acetazolamide (carbonic anhydrase inhibitor) → reduces HCO3- concentration
  • ******Hemodialysis or HCl infusion for life-threatening metabolic alkalosis******

Question 219

Tx of Respiratory Acidosis

Answer 219

represents ventilation failure or impaired control of ventilation

• hypoxemia + hypercapnia
• severe, acute respiratory acidosis =
  
  • HA, blurred vision, restlessness and anxiety, tremors, somnolence, and/or delirium
• Tx = identify cause and tx that:
  
  • opiate/opioids → naloxone
  • acute bronchospasm/asthma → bronchodilators
  • assisted ventilation and mod-severe acidosis → BiPAP
  • NOTE: NaHCO3 may actually worsen acidemia due to increased CO2 generation so do NOT use this
• Goals:
  
  • careful monitoring of pH
  • maintain oxygenation
  • improve alveolar ventilation

Question 220

Tx of Respiratory Alkalosis

Answer 220

represents hyperventilation

• sxs: irritability of central and peripheral nervous system
  
  • light headedness, altered consciousness, cramps, syncope
  • severe cases: HypoPhos shifts from ECF to ICF
• tx: identify cause and tx accordingly
  
  • for mild-moderate severity in spontaneously breathing pts → no specific tx
  • severe alkalosis:
    
    • rebreathing
      
      • rebreathing mask, or paper bag
      • mechanical ventilation
      • high level sedation or paralysis is a good option

Question 221

Hypokalemia Tx

Answer 221

When to tx? <3.5 mEq/L and/or pt is symptomatic

• treatment:
  
  • oral: K-chloride, KPO₄, K-acetate, K-citrate, k-gluconate
    
    • IV: if >10 mEq/L should be monitored via telemetry
  • other: diuretic induced (spironolactone- K+ sparing diuretic)
    
    • correct hypomagnesemia
      
      • ****low magnesium makes body resistant to K+ replacement, so tx mg deficiency first or concurrently*****
    • correct acid-base imbalance

Question 222

Hyperkalemia Tx

Answer 222

• Symptomatic (urgent/emergent)
  
  • IV calcium to stabilize the heart membrane
  • insulin +/- glucose/dextrose to temporarily push K+ back into the cell
  • albuterol to also temporarily push K+ back into the cell
  • Sodium bicarb to be considered to tx acidosis
  • Eliminate Source: IV, total parenteral nutrition (TPN), tube feeds, oral supplements, K sparing diuretics
• Symptomatic:
  
  • sodium polystyrene sulfonate (Kayexelate) → binds potassium, slower onset, but duration of 4-6 hours (constipation though…)
  • Loop diuretics (lasix)
• Asymptomatic;
  
  • eliminate source
  • kayexelate (sodium polystyrene sulfonate) → binds potassium
  • loop diuretics

Question 223

Hypokalemia Etiology, S/sxs, Dx, & Tx

Answer 223

• potassium <3.5 mEq/L
• Etiology:
  
  • increased urinary/Gi losses
    
    • diuretic therapy, vomiting, diarrhea; renal tubule acidosis
  • increased intracellular shifts
    
    • metabolic acidosis, beta-2 agonists, hypothermia, insulin, aldosterone
  • hypomagnesemia
  • decreased intake→ rare
• S/sxs:
  
  • neuromuscular: severe muscle weakness, rhabdomyolysis
  • nephrogenic DI: polyuria (affects renal concentrating ability), cramps, n/v, ileus (obstruction of ileum
  • cardiac: palpitations, arrhythmias
  • no change in mental status
• Dx:
  
  • BMP: potassium <3.5mEq/L, magnesium, glucose, and bicarb should be ordered in work up
  • Spot Urine K > 20 mmol/L (renal cause)
  • Spot Urine K < 20mmol/L (non-renal cause)
  • ECG findings: T-wave flattenedfollowed by a prominent u-wave
• Tx: potassium replacement→ KCl oral if possible, IV KCl if rapid/severe tx needed
  
  • potassium sparing diuretic (spironolactone, amiloride)
  • check for hypomagnesemia (need to correct for this 1st or concurrently)
  • ***Use non-dextrose IV solutions b/c dextrose will cause spike in insulin release which will cause more K to shift into the cells ***

Question 224

Hyperkalemia Etiology, S/sxs, Dx, & Tx

Answer 224

serum potassium > 5-5.5mEq/L

• Etiology:
  
  • decreased renal excretion: acute/chronic renal failure
  • decreased aldosterone → hypoaldosteronism, adrenal insufficiency
  • Meds: K+ supplements, K+ sparing diuretics (thiazides, spironolactone, amiloride), ACEI/ARBs, digoxin, beta-blockers, NSAIDs, cyclosporin
  • Cell lysis → rhabdomyolysis, hypovolemia, thrombocytosis, tumor lysis syndrome
  • K redistribution → metabolic acidosis
• S/sxs:
  
  • neuromuscular: weakness (progressive ascending), fatigue, paresthesias (tingling), flaccid paralysis
  • cardiac: palpitations and cardiac arrhythmias
  • GI: abdominal distention, diarrhea
• Dx:
  
  • ECG: peaked T-waves, prolonged QRS, St depression
  • BMP: potassium > 5.0 mEq/L, glucose and bicarb part of the workup +/- CBC (hemolysis)
• Tx: repeat blood draw to ensure that increased K isnt from hemolysis (since venipuncture may cause this)
  
  • IV Calcium Gluconate → stabilize the cardiac membrane → only for severe symptoms, K >6.5, + significant ECG findings
  • → insulin with glucose/dextrose → insulin shifts K+ intracellularly
  • Kayexalate (sodium polystyrene sulfonate) → enhances GI excretion of K+, lowers total K+
  • SABA: albuterol (4-8x dosing for asthma)
  • loop diuretics; dialysis if severe

Question 225

Hypernatremia Etiology, S/sxs, Pe, Dx, & Tx

Answer 225

• serum sodium >145 mEq/L
  
  • caused by increased free water loss, hypotonic fluid loss, or hypertonic sodium gain
• Etiology: diabetes insipidus, diarrhea, sweating, burns, fever, insensible loss
  
  • → infants, elderly, debilitated pts or impaired thirst mechanism → water intake decreased
• S/sxs: PRIMARILY CAUSED BY SHRINKAGE OF BRAIN CELLS → dehydration
  
  • thirst = most common initial sx
  • confusion, lethargy, disorientation, fatigue, N/V, muscle weakness, seizures, coma, brain damage resp. arrest
• PE: dry mouth, mucus membranes, decreased skin turgor, tachycardia, hypotension
• Dx: serum studies → serum Na, urine osmolarity, serum osmolarity, assess volume status
• Tx: hypotonic fluids: pure water oral, D5W, 0.45%NS,
  
  • isotonic fluids if hypovolemic to replenish volume then hypotonic fluids
  • if Central diabetes insipidus → desmopressin (synthetic analog to ADH)
  • renal diabetes insipidus → NSAIDs (constrict afferent renal arteriole and reduce GFR)
  • rapid correction (>0.5mEq/L.hr) → can results in Cerebral edema

Question 226

Hyponatremia Etiology, S/sxs, PE, & Dx

Answer 226

serum sodium <135 mEq/L

• due to increased free water
• clincially significant → hypotonic hyponatremia
• etiology:
  
  • hypertonic hyponatremia → due to hyperglycemia or mannitol infusion
  • Isotonic Hyponatremia → lab error due to hyperproteinemia or hypertrigliceridemia
  • Hypotonic Hyponatremia →
    
    • hypovolemic → renal volume loss (diuretics, ACEI); extraneal volume loss → GI loss (diarrhea & vomiting), burns, fever
    • Isovolemic: SIADH, hypothyroidism, adrenal insufficiency water intoxication, MDMA, tea and toast syndrome
    • hypervolemic: edematous states → CHF, nephrotic syndrome, cirrhosis
  • S/sxs: primary caused by cerebral edema → confusion, lethargy, disorientation, fatigue, N/V, cramps, Seizures, coma, respiratory arrest
  • PE:
    
    • hypervolemia → edema, JVD, HTN; decreased HCT, serum protein, BUN:creatinine
    • hypovolemia→ poor skin turgor, dry mucus membranes, flat neck veins, hypotension; increased hct, serum protein, BUN:creatinine ratio >20:1
  • Dx:
    
    • 3 steps:
      
      1. measure serum sodium
      2. serum osmolality (275-295 mOsm/kg)
      3. assess volume status (if hypotonic/decreased osmolality)

Question 227

Hemophilia

Answer 227

X-linked recessive inheritance clotting factor disorder

• Hemophilia A: factor VIII decrease → “Aight”
• Hemophilia B: decreased clotting factor IX
• Normal Factor Activity: 50-150%
  
  • mild: 6-49% (Bleeding during surgery)
  • moderate: 1-5% (occasional bleeding)
  • Severe: <1% (spontaneous bleeding)
• S/sxs:
  
  • hemarthrosis (bleeding in joint)
    
    • main sxs = excessive bleeding
• Diagnosis: increased PTT, normal PT, normal platelets and function
  
  • → corrected with mixing study
    
    • if PTT is NOT corrected with mixing studies = indication of lupus anticoagulant or factor inhibitor
  • most specific test: functional assay for factor VIII or IX
• Tx: replacement for depleted factors
  
  • avoid situations that cause bleeding
  • avoid certain drugs that interfere with platelet function (NSAIDs and aspirin)

Question 228

Von Willebrand Disease

Answer 228

Autosomal Dominant → most common genetic bleeding disorder clotting factor disorder

• missing protein for platelet function (usually hangs out in the endothelium of the blood vessels and is important for factor VIII transport → platelets cannot adhere to vessel at site of injury → bleeding doesn’t stop as quickly as it should
• hormonal changes, stress, pregnancy, inflammation, and infection can stimulate vWF production
• S/sxs: hx and family hx of bleeding, bruising easily, increased menstrual bleeding, no hemarthrosis, petechiae, bleeding with minor injury
• Dx:
  
  • decreased vWF and decreased Factor VIII
  • normal CBC, normal platelet count, and increased bleeding time
    
    • → normal or prolonged PTT with normal PT
• Tx: DDVAP (desmopressin)
  
  • if excessive bleeding → transfusion of concentrated blood clotting factors containing vWF

Question 229

What causes a high aPTT?

Answer 229

activated partial thromboplastin time

measures the intrinsic pathway (slower)

• Intrinsic Pathway Factors: XII, XI, IX, VIII
• aPTT is the time in seconds for a fibrin clot to form: measures the function of factors VIII, IX, and XI
• Causes of a high aPTT:
  
  • heparin
  • decreased factor (VIII, IX, XI), vitamin K, liver disease
  • consumption: inhibitor, DIC

Question 230

Alpha-Thalassemia

Answer 230

Autosomal Recessive hemoglobinopathy

Hypochromic microcytic anemia

• S/sxs:
  
  • carrier: 1 deletion = asymptomatic
  • alpha thalassemia minor: 2 deletions = mild anemia, microcytic hypochromic
    
    • cis deletion for asians
    • trans deletions for AAs
  • alpha thalassemia major: 3 deletions: symptomatic → SPLENOMEGALY, MCHC, anemia, some need transfusion periodically
  • Hemoglobin Bart’s Hydrops Fetalis: 4 deletions = incompatible with life
• Dx: decreased MCV, low hgb, HIGH RBC, normal ferritin, normal TIBC and a (+) HgB electrophoresis
  
  • peripheral smear: target, heinz bodies “Golf ball” looking cells and teardrop cells, microcytic
  • hgb electrophoresis: normal hgb rations in adults with 1-2 gene deletions, detects hgbH with 3 gene deletion
• Tx: for alpha thal minor → no tx
  
  • for alpha thal major → can do splenectomy if severe anemia or splenomegaly

Question 231

Beta-Thalassemia

Answer 231

Autosomal recessive hemoglobinopathy

hypochromic microcytic anemia

• Beta Thal major: 2 of 2 beta genes damaged = significant organ damage, transfusion dependent anemia, excess alpha chains, stable as monomers, no precipitation in RBC
• Beta Thal Minor: 1 of 2 beta genes are damaged = mild-mod anemia
• S/sxs:
  
  • thrombosis = vascular disease
  • ineffective erythropoiesis → splenomegaly, hepatomegaly, bone pain
  • hemolysis = iron deposition and gallstones → endocrine dysfunction, cirrhosis, heart failure
• Dx:
  
  • very high RBC, low MCV, very hypochromic, normal ferritin, normal to low reticulocyte count, normal RDW
  • peripheral smear: target and teardrop cells, basophilic stippling; nucleated RBCs → suspect thalassemia in pts with microcytosis and normal iron with increased RBC count
  • hgb electrophoresis:
    
    • trait (minor): increased HgA2 or increased HgbF and decreased HgbA
    • Major (Cooley’s): increased HgA2 or increased HgbF (up to 90%) and little to no HgbA
• Tx:
  
  • beta thal major: transfusion hgb 11-12
    
    • folic acid daily
    • luspatercept: RBC maturation agent
    • splenectomy
    • bone marrow transplant (for severe cases)
    • iron chelation daily (need to prevent iron overload)

Question 232

Acute Leukemias Overview

Answer 232

• onset over few weeks
• symptomatic
• immature WBCs
• decreased hgb and platelets
• need tx
• risk of death

Question 233

Chronic Leukemias Overview

Answer 233

• onset over months -years
• minor sxs
• excess mature WBCs
• normal hgb and platelets
• may need tx
• chronic disease

Question 234

Acute Lymphocytic Leukemia

Answer 234

• Population: children, boys>girls, hispanics, 2-5yo
• Pathophys: overpopulation of immature WBCs (lymphoblasts) overtake normal hematopoiesis
• Pearl: CHILD+Lymphadenopathy + bleeding + fever + bone marrow > 20% blasts
• S/sxs: Pancytopenia → fever & infx (leukopenia); bleeding, petechiae, purpura (thrombocytopenia); Pallor & fatigue (Anemia)
• Dx: bone marrow aspiration >20% blasts
  
  • flow cytometry test: tells you subtype of leukemia
  • WBCs 5-100K, decreased hgb and platelet
• Tx: combination chemo → highly responsive with a remission >90%
  
  • can do stem cell transplant if relapse

Question 235

Chronic Lymphocytic Leukemia

Answer 235

• Population: adults: most common form of leukemia in adults (~50yo; men > women) Mature B cell clonal malignancy → lymphocyte normal range 20-40%
• S/sxs: often asymptomatic, fatigue, weight loss, sxs related to pancytopenia
  
  • → lymphadenopathy, splenomegaly
• Dx: peripheral blood smear: Lots of B-cells, limited other leukocytes. “smudge cells”
  
  • WBC > 20K
  • Absolute lymphocyte count > 5000 (5K)
• Tx: chemo, observation if indolent

Question 236

Myelodysplasia

Answer 236

• Pre-malignant, leukemic disorder
• Risk factors: age >65, radiation therapy, chemo, tobacco, mercury/lead exposure
• S/sxs: often asymptomatic: pancytopenia → easy bruising, bleeding, frequent infx & fatigue
• Dx: bones marrow biopsy → dysplastic bone marrow = hallmark → increased myeloblasts <20%
• Tx: goals are sx improvement and prevention of progression to AML (blasts >20% in bone marrow)
  
  • some may need intermittent blood or platelet transfusions and EPO

Question 237

Acute Myelogenous Leukemia

Answer 237

• Pearls: most common presentation → blasts + Auer rods in adult pts t(15:17)**
  
  • major of pts > 50yo
  • Auer rods associated with DIC
• S/sxs: anemia, bleeding, bruising, bone pain, thrombocytopenia, neutropenia
  
  • TUMOR LYSIS SYNDROME
• PE: splenomegaly, gingival hyperplasia
• Dx: >20% of myeloblasts in bone marrow = GOLD STANDARD, + myeloblasts with auer rods
  
  • CBC: normocytic, normochromic anemia with normal or decreased reticulocyte count
• Tx: combo of chemo + bone marrow transplant
  
  • tumor lysis syndrome → allopurinol or rasburicase

Question 238

Chronic Myelogenous Leukemia

Answer 238

BCR-ABL translocation t(9:22)(Philadelphia gene)

• S/sxs: fatigue, abdominal pain, night sweats, weight loss
  
  • → splenomegaly
• Dx: CBC full spectrum of WBCs, hgb and MCV = normal, platelets = slightly elevated
  
  • BCr-abl fusion
• Tx:
  
  • imatinib = tyrosine kinase inhibitor for philadelphia + → they inhibit philadelphia chromosome tyrosine kinase activity and myeloid leukemic cell proliferation
  • hematopoietic stem cell transplant = most effective cure

Question 239

Hodgkin’s Disease

Answer 239

• general: most common type of lymphoma, age: bimodal 20s & 50s, associated with EBV infx
• S/sxs: B-cell sxs are NOT common→ fever, night sweats, weight loss, fatigue (sxs due to cytokine release from B-cells)
  
  • Pel-Ebstein Fever: cyclical high fever q 1-2 weeks
• PE: painless lympha, especially of upper body lymph nodes (but may worsen with EtOH ingestion)
  
  • if solitary lymph node present > 30 days with no pain and no change → needs to be biopsied
  • contiguous spread (owls fly to the next tree)
• Dx: Reed-Sternberg cells = Pathognomonic → B-cell proliferation with bilobed or multilobed nucleus “Owl Eyes” -→ OWL’s HOOT
  
  • Excisional biopsy of lymph node, may need bone marrow
• Tx: excellent 5 year cure rate (60%)
  
  • chemo + radiation
    
    • ***stage predicts outcome***: Ann Arbor Staging: stage I-II single side of diaphragm; stage III-IV both sides of diaphragm
  • SEs of tx: cardiac disease if mediastinal radiation

Question 240

Multiple Myeloma

Answer 240

• most common primary tumor of the bone/bone marrow in pts >50
  
  • all myeloma has prior MGUS stage, but only 1%/yr of MGUS pts develop myeloma
• Malignant clonal disorder of ***plasma cells*** → overproduction of IgG or IgA
• S/sxs: CRAB:
  
  • hypercalcemia
  • Renal failure
  • Anemia
  • Bone pain (atraumatic fractures
• Pe: punched-out lytic bone lesions
• Dx: serum protein electrophoresis → to determine clonality: monoclonal immunoglobulin
  
  • urine protein electrophoresis → Ig light chains (Bence Jones Protein)
  • RBC rouleaux formation
• Tx: median survival = 10 years
  
  • complications of infx, renal failure, spinal cord compressionb
    
    • chemo +/- stem cell transplant
    • 3 med combo: revlimid (oral) + decadron (oral) + bortezomib (SQ) → disrupts protein production

Question 241

Virchow’s Triad

Answer 241

1. endothelial injury (surgery, inflammation, chemo, cancer)
2. abnormal blood flow (injured limb, sedentary, travel)
3. hypercoagulability (estrogen, cancer, hereditary)