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CCP - Semester 2 > Quick n dirty Patho > Flashcards

Quick n dirty Patho Flashcards

1
Q

Pneumothorax definition

A

gas within the pleural space

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2
Q

PTX hx

A

dyspnea, pleuritic chest pin, spontaneous, trauma, iatrogenic

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3
Q

PTX Physical

A

tachypnea, tachycardia, decreased AE, hypoxemia, high PIP + pPlats, subcutaneous air, hyperresonance, (obstructive findings: JVP, hypotension, tracheal deviation)

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4
Q

PTX imaging

A

CXR –> white visceral pleural line on chest radiograph, wont see bronchovascular markings beyond the white line
POCUS –> No lung sliding, lung point, lung pulse M-mode barcode

easier found on Ct than CXR, also can turn the cxr opposite contrast

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5
Q

PTX Tx

A

chest tube, or leave if not significant

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6
Q

Massive HTX definition

A

1500ml release, or 200ml over 2-4 hours =

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7
Q

Massive HTX tx

A

emergency thoracotomy

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8
Q

HTX defintion

A

blood within the pleural space is termed hemothorax. often from aortic rupture, Myocardial rupture, injuries to hilarity structures, lung parenchyma, or intercostal vessels

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9
Q

HTX imaging

A

CXR - whiteout

POCUS - anechoic fluid ++spine sign

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10
Q

HTX tx

A

chest tube 4/5th intercostal

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11
Q

Pulmonary Embolism definition

A

PE is a form of venous thromboembolism that obstructs the pulmonary artery or one of its branches by material that originated elsewhere in the body

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12
Q

PE hx risk/clinical

A

risk: hypercoag, vessel injury, venous stasis.
clinical: dyspnea, CP, cough, dvt, shock, sudden death (hemoptysis associated with PE infarction )

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13
Q

PE imaging

A

CT or VQ scan

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14
Q

PE Tx

A
  • UFH
  • very conservative volume optimization
  • norepi, dobutatmine +/- e[I
  • embolectomy
  • tPa (for hemodynamically unstable patients)
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15
Q

Massive Hemoptysis definition

A

life threatening hemoptysis when hemoptysis results in life-threatening event including significant airway obstruction, significant abnormal gas exchange, or hemodynamic instability

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16
Q

massive hemoptysis hx

A

bronchiectasis, cystic fibrosis, TB, myectomas, lung cancer

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17
Q

massive hemoptysis imaging

A

bronchoscope, CXR, CT-A

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18
Q

massive hemoptysis tx

A

large bore ETT, normal vent settings usually.

  • bad lung down
  • bronchial alveolar lavage
  • single lung ventilation potentially
  • double lumen ventilation
  • bronchial blockade
  • reverse coagulation
  • Inhaled TXA
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19
Q

CAP definition

A

CAP is defined as an acute infection of the pulmonary parenchyma in a patient who has acquired the infection in the community

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20
Q

Dx of CAP

A

CAP generally required the demonstration of an infiltrate on chest radiography in a patient with clinical compatible syndrome

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21
Q

PNA hx

A

fever, cough, pleurite chest pain, sputum production, tachypnea

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22
Q

PNA imaging

A

infiltrates on plain film is considered the gold standard for dx pneumonia when clinical and microbiologic features are supportive

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23
Q

PNA TX

A

empiric treatment directed at the most likely pathogens to start

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24
Q

RV spiral of death

A

RV dilation, TV insufficiency, RV wall tension, Neurohormonal activation, myocardial inflammation, RV O2 demand, RV ischemia, decreased contractility, decreased LV preload, decreased systemic BP, decreased RV coronary perfusion, decreased RV O2 delivery —> cardiogenic/obstructive shock –> death

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25
Q

causes of severe RV afterload

A

PE, Severe PH

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26
Q

RV failure imaging

A

parasternal long n short, CT

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27
Q

RV failure potential tx

A

potentially diuresis, norepinephrine + dob, +e/- epi

-not more fluids

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28
Q

Acute respiratory distress syndrome definition

A

Berlin’s criteria:
1 week resp symptoms, with bilateral lung infiltrates that are non-cariogenic in origin. then modified into PF ratios for severity

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29
Q

ARDS pathophysiology, big boy.

A

Healthy lungs regulate the movement of fluids to maintain a small amount of interstitial fluid and dry alveoli.
In ARDS, this regulation is interrupted by lung injury, causing excessive fluid in both the interstium and alveoli.

Consequences include: **impaired gas exchange **decreased compliance ** increased pulmonary arterial pressure

++deeper++
ARDS is a consquence of an alveolar injury producing diffuse damage. This injury causes release of IL-1,IL6,IL8, and TNF damaging alveolar and capillary epithelium. Damage to the capillary endothelium allows proteins to escape from the vascular space. The oncotic gradient that favours resorption of fluids lost and fluid poors into the interstium, overwhelming the lymphatic system.

Consequences include: **impaired gas exchange **decreased compliance ** increased pulmonary arterial pressure

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30
Q

3 common causes of ARDS

A

sepsis, PNA, trauma

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31
Q

ARDS treatments

A

VILI, use of sedatives, potentially paralytics, hemodynamic mgmt, nutritional support, glucose control, DVT, prophylaxis, and GI bleeding, conservative fluids

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32
Q

Asthma definition

A

A common chronic disorder of the airways that is complex and characterized by variable and recurring symptoms, airway obstruction, bronchial hyper responsiveness and an underlying inflammation

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33
Q

Asthma pathophysiology

A

Reversible airway inflammation in the setting of acute IgE mediated inflammation and constriction. Basophils, mast cells and eosinophils degranulate to release histamine and increased mucus production and decrease lumen of bronchiole. Complicated by smooth muscle constriction

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34
Q

critical Asthma Hx

A
  • previous icu admins
  • ≥2 non-icu hospitalization in the past year
  • ≥3 ED visits in the past month for asthma exacerbation
  • chronic us of oral corticosteroids
  • medication non-compliance
  • using ≥2 SABA pressurized MDI month
  • poverty with no access to health care
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35
Q

asthma imaging

A

CXR = hyperinflated, flattened hemi-diaphragms

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36
Q

Asthma Treatment

A
  • inhaled IV steroids (decreases IgE)
  • ventolin (B2 agonist)
  • atrovent (anti-muscarinic)
  • NIPPV
  • High flow for MV (consider ZEEP )
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37
Q

Asthmatic Dynamic hyperinflation ( I can condense this more…)

A
  1. expiration usually occurs as passive movement
  2. resistance to airflow (bronchospasm) results in decreased expiratory flow
  3. decreased expiratory flow results in longer time required to expire the full Vt
  4. if expiration is interrupted before its natural end by the next inspiration, some unexpired residual gas remains in the chest
  5. this gas exerts a pressure onto the respiratory circuit
  6. as a result the alveolar pressure at the end of expiration is higher than zero (zero being atmospheric)
  7. this process of incomplete emptying is called dynamic hyperinflation, and the positive pressure alveolar pressure is called intrinsic PEEP or auto-PEEP
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38
Q

AECOPD defintion

A

AECOPD has 2 of the following

1) worsening dyspnea
2) increased sputum production
3) increased purulence

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39
Q

COPD patho

A

1) Bronchioles in COPD lose elastic fibers and are destroyed and become collapsible.
2) additionally, destruction of the alveoli and lose surface area
3) there’s an obstruction because air cannot get out of the lung. The alveoli are all destroyed and large sacs of air, and can’t get back into the obstructed, collapsed bronchioles

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40
Q

COPD imaging

A

CXR - very dark, hyperinflated, flattened hemi-diaphgrams, potentially increased pulmonary vasculature (PH) +/- blebs

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41
Q

COPD tx

A 
ventolin
atrovent
steriods
abx 
NIPPV
MV
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42
Q

AutoPEEP in COPD

A
  • alveoli remain inflated at end-expiration due to obstruction, so alveolar pressure is greater than atmospheric pressure
  • In the absence of inspiratory effort, intrapleural pressure approximates alveolar pressure.
  • AutoPEEP increasing WOB to overcome the positive pressure in the alveoli during inspiration, the diaphragm must generate enough negative pressure to exceed the auto-PEEP and transmit negative pressure to the central airways, generating airflow
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43
Q

Recognizing DHI

A

1) High autoPEEP (check ur fucking vent)
2) Failure of expiratory flow to return to zero before next breath (waveforms)
3) Trigger dyssynronchy
4) Inspriration volumes&raquo_space; than expiratory volumes significantly

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44
Q

Treatment of DHI in COPD

A
  1. change vent settings (decrease RR, decrease I-TIME, prolong expiratory time)
  2. Reduce demand (reduce anxiety, pn, fever)
  3. reduce flow resistance
    (suction, use large ETT, bronchodilator)
  4. counterbalance expiration flow limitations
    (external PEEP)
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45
Q

Caurda Equina Syndrome

A
  • *decreased bowel
  • *decreased bladder
  • *decreased sexual function

Injury distal to L2 spinal cord, caused by compression/trauma or lumbar disc. Damage to multiple nerves of the caudal equina

Treatment: surgical decompression within 48 hours

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46
Q

Brown Sequard Syndrome

A

Ipsilateral loss of:

1) upper motor neuron weakness
2) ipsilateral hemiparesis
3) loss of proprioception

Contralateral loss of:
1) pain 2) temperature

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47
Q

Central cord syndrome

A 
MUDE
Motor loss
Upper extreme > lower loss
Distal worse than prox
-extension injuries
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48
Q

Dorsal column

A

All sensory (spine to cortex)

  • proprioception
  • deep touch
  • tactile sensation
  • vibration
  • fine sensory

goes to ascending up dorsal tract, decussation at medulla then hits thalamus then goes to cortex

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49
Q

spinothalamic

A

pn/temp

crosses over 1-2 vertebrae above

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50
Q

Somatic reflexes

A

automatic, reflex arc is felt from the afferent spinal nerve then at the level of the vertebra it relays information to the intraneuron area which correlates to a motor efferent response

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51
Q

upper motor neuron

A

CNS/spinal cord

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52
Q

lower motor neuron

A

PNS

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53
Q

How does PEEP effect the Left heart

A

1) Decrease preload (decreased venous return)

2) Decreases LV afterload.
(By decreasing LV unloading. Decrease LV afterload due to baroreceptor response from increased intraaortic pressure)

3) Decreased SV due to intreventricular dependence
4) decreased MVO2
5) increased pressure gradient from thorax to periphery
6) increased hydrostatic displacement of alveolar edema

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54
Q

summary effects of PEEP on RV

A

1) decrease venous return
2) decreased hypoxia pulmonary vasoconstriction
3) increased pulmonary vasculature resistance due to vascular compression

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55
Q

Increased PIPs with normal pLats

A

Resistance Issue.

worsening asthma, obstruction of ETT, excessive airway secretions, clogged HME, small ETT, high flow rate

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56
Q

Increased PIP with elevated pPlats

A

PTX, ARDS, PNA, Pulmonary edema, atelectasis, pleural effusion, bronchial intubation.

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57
Q

asthma vent settings for:

1) mode
2) fio2 target
3) PIP target
4) pPlat
5) PEEP
6) VT
7) vCalc 80-100L/min
8) RR
9) I:E ratio
10) expiratory time

A 
Mode	AC-V
FiO2	Adjust to SaO2 of >92%
PIP	Adjust to level above peak airway pressures. Caution at PIP >50 cmH20
pPlat	<30cmH20
PEEP	ZEEP if paralyzed and sedated. Some patients require small amounts of PEEP to match intrinsic PEEP. However, intrinsic PEEP les than COPD
VT	4-8ml/kg
vCalc	80-100L/min
RR	6-10 BPM
IE	1:4, 1:5
Expiratory Time	4-5 seconds
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58
Q

5 effects of PEEP on pulmonary system

A
  1. increased FRC
  2. Decreased in intrapulmonary shunt
  3. Reduction of alveolar opening and closing (preventing atelectacto-trauma VILI)
  4. increased in intrathoracic pressure (decrease venous return, decrease in LV transmural pressure -> afterload)
  5. Distention of normally aerated alveoli
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59
Q

Sepsis induced caridomyopathy

A

In sepsis induced cardiomyopathy, the myocardium is functionally and structurally injured by inflammatory cytokines and mitochondrial dysfunction.

Its characterized by: decreased EF, LV dilation and a recovery time of 7-10 days

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60
Q

Glucose targets in sepsis

A

4.5-6 mmol/L as per NICE-SUGAR trial

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61
Q

Sepsis Physical

A
  1. bend the neck (meningitis)
  2. listen to all lung zones (PNA)
  3. listen for murmurs (endocarditis)
  4. palpate RUQ (billiary)
  5. palpate flanks (nephritis)
  6. Palpate belly (perforation/ileus)
  7. examine the skin (necrotizing fasciitis)
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62
Q

reasons to treat seizures prophylactically, maybe.

A
  1. hx of seizures/current seizures
  2. temporal lobe pathology
  3. depressed skull #
  4. penetrating trauma to cranial vault
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63
Q

CCP goals of care for TBI

A
  1. cerebral blow flow
  2. venous outflow
  3. brain parenchyma
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64
Q

when to consider ETT with SCI

A
  1. use of spinal access muscles (shrug shoulders/tracheal tugging)
  2. no bicep curls
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65
Q

Sepsis approach

A
  1. source control
  2. Abx
  3. Optimize VO2/DO2
  4. Adjuncts ( steroids, Vitamin C)
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66
Q

how does PPV increase LV preload

A

preload can be increased because of pushing of fluid from west zone 3 to return to the heart (depend on fluid status)

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67
Q

How does PPV decrease LV afterload

A

by increasing intrathoracic pressure, creating a bigger gradient from the thorax to periphery.

also, decrease in LV afterload due to baroreceptor response to increase intrathoracic pressure on the aorta

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68
Q

equation of EF

A

SV/EDV X 100

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69
Q

Oxygen Consumption equation

A

CO= CaO2-CvO2

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70
Q

LaPlace’s Law

A

• Wall tension (T) = Transmural Pressure (P) x Radius ( r ) / 2xWall thickness (h)
Wall tension relates to work that the heart has to do

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71
Q

End organ perfusion markers

A

aloc, lactate, urine output cap refill, look at their trends, scvo2

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72
Q

Atherosclerosis pathophysiology

A
  1. LDL can deposit in the tunica intimacy, and then become oxidized.
  2. Oxidized LDLs activate the endothelial cells to attract WBCs
  3. Monocytes enter the tunica intimacy and become macrophages, and macrophages take up these oxidized LDLs and then become foam cells.
  4. Foam cells eventually die, spilling out their lipid content, which grows the plaque and increases its pressure.
  5. The plaque then can rupture and cause coagulation, causing thrombus, impeding blood flow.
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73
Q

STEMI medical mgmt

A
  • PCI/lysis
  • Anticoagulation (UHF, LMWH)
  • Dual antiplatelet (ASA, P2Y12 [Ticagrelor/plavix])
  • Beta Blockers
  • ACE-Inhibtors/ARBs
  • Statins
  • Potassium >4 /Mag levels >1
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74
Q

Rescue PCI

A

after failed lysis, st resolution <50%, ongoing ischemic changes, shock

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75
Q

Facilitated PCI

A

Use thrombolysis to “facilitate” a smoother PCI

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76
Q

Elevated troponin without ECG changes

A

type 2 MI, supply and demand.

increased demand from systemic critical illness

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77
Q

MI complications

A 
DARTHVADER
D-eath
A-rrthymia
R-upture
T-amponade
H-eart Failure
V-alve disorder
A-neurysm
D-dressler Syndrome
E-mbolism
R-egurgitation/reoccurance
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78
Q

Heart Failure triple therapy

A
  1. ACE-I
  2. Beta Blockers
  3. Spironolactone
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79
Q

Acute decompensated Heart failure Forrester classification

A
  1. Dry + Warm (adequately perfused, hemodynamically compensated)
  2. Dry + Cold (Hypoperfused and hypovolemic)
  3. Wet + warm (congestion but well-perfused)
  4. Wet + Cold (congested and hypotensive)
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80
Q

pressures of the heart

A

Think of it as change: 5, 10, 25, 100

or

RA= 2-8
RV=  15-30/2-8
PA=  15-30/4-12
LA=2-10/
LV=100-140/3-12
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81
Q

STEMI mimiks

A

ELEVATION.

E-electrolytes (hyperK)
L-left bundle branch
E - (BER)
V - Ventricular hypertrophy
A- Arrhythmia/aneurysm (VT/brugada/LV-An)
T-takotsubo, TBI
I-Infarct MI, Injury(contusion)
O- Osborn wave (hypothermia)
N- Non-athersclerotic vasospasm (prenzmental)
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82
Q

Dilated cardiomypathies causes

A
  • Genetic
  • Infection
  • Systemic Immune-Mediated Disease
  • Toxic and overload
  • drugs
  • Endocrine/metabolic
  • Peripartium
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83
Q

Dialated cardiompathy treatments

A

adress underlining cause, treat heart failure, prevent arrthymia, prevent thromboembolic events, heart transplant

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84
Q

HCM causes and characteristics

A

Distinct from ventricular hypertrophy as HCM is disproportionally effects the SEPTUM

familial, symptoms related to diastolic dysfunction and LV outflow obstruction

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85
Q

Whats HCM with SAM

A

HCM with Systolic Anterior Motion. Where the mitral valve becomes sucked back into the LVOT during systole, physically obstructing flow. Sounds awful.

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86
Q

Treatment for Aortic Stenosis

A

Preload: increased
Afterload: normal
HR: Decreased
Contractility: Increased

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87
Q

Treatment of Aortic Regurgitation

A

Preload: normal
afterload: decrease
HR: high normal
Contractility: increase

88
Q

Tx of Mitral stenosis

A

Preload: normal
Afterload: normal
HR: Decrease
Contractility: normal

89
Q

Tx of mitral regurg

A

preload- decrease
afterload- decrease
HR- high normal
Contractility - Increase

90
Q

Rheumatic heart disease

A
  1. Group-A Strep (GAS) pharyngitis leads to both an innate and adaptative immune response
    1. The immune response gets activated leading to the development of cross-reactive antibodies and cross-reactive T-cells which effect the joints, heart, skin and brain.
    2. Scaring, stretching of the left-sided heart are typically effected. Causing either stenosis or regurgitation
91
Q

Autonomic factors affecting HR

A
  • autonomic innervation
  • hormones
  • fitness level
  • age
92
Q

Factors affecting Stroke volume

A

-heart size
-fitness level
-gender
-contractility
-duration of contraction
-preload
(EDV)
-afterload (resistance)

93
Q

ACA perfuses

A

frontal lobe

94
Q

MCA perfuses

A

blood flow to the frontal, partial, temporal lobe

95
Q

PCA perfuses

A

supplies blood flow occipital lobe

96
Q

ACA stroke syndrome

A

Will give you contralateral leg weakness only

97
Q

MCA stroke syndrome

A

right: arm, face, contralateral + neglect
left: arm, face, contralateral and speech

98
Q

internal capsule

A

everything from the motor and sensory - face, arm, and leg weakness contralateral

99
Q

post arrest targets

MAP, CO2, PaO2, Hb and temp

A 
MAP 80
PaO2 80-100
PcO2 35-40
Hb- 90
temp 34-36
100
Q

SCI map goals

101
Q

Ischemic Stroke lysed n non-lysed

A

pre-post lysis - SBP 180

non-lysed - 220

102
Q

AAA targets and treated with

A

SBP 100-120 mmHg, HR 55-60. Labetalol and nitroprusside

103
Q

SAH, Epidual, intercapsle, ischemic cva with hemorrhagic transformation

104
Q

Undifferentiated TBI

105
Q

Coagulation goals for neurotrauma

A
  • INR < 1.5
  • Platlets > 100 (platlets)
  • PTT <40 (FFP)
  • Fibrinogen > 1 (Cyroprecipitate)
  • Hb >90g/L
  • warfarin = octaplex is supra-therapeutic.
  • Heparin reversal = protamine

-Inquire about TXA within 3 hours for cerebral contusion/subdural hematoma

106
Q

Causes of increased right sided afterload

A
  1. Left-sided heart failure (increasing pulmonary vasculature pressures)
  2. End stage COPD
  3. PE
  4. Obstructive sleep apnea
107
Q

HFpEF

A

Diastolic Failure, hard ventricle, normal EF

108
Q

HFrEF

A

Systolic failure

109
Q

Rheumatic Heart Disease patho

A
  1. Group A Strep (GAS) pharyngitis leads to both an innate and adaptive immune response.
  2. The immune response gets activated leading to the development of cross-reactive antibodies and cross-reactive T cells which effects the joints, heart, skin and brain.
  3. Scaring, stretching of the left-side heart are typically effected. causing either stenosis or regurgitation.
110
Q

Cardiac Tamponde

A

-Hemodynamically unstable
-Narrow Pulse pressure
-RV collapse
-Pulsus Paradoxus, >10mmHg and during inspiration - relating to physiologic interdependence
-becks triad
-low voltage ECG
Pocus) 1 pericardial 2. RV collapse 3. dilated IVC

111
Q

Pericarditis treatment

A

Mostly symptom mgmt, NSAIDS

112
Q

Infectious endocarditis casuses

A

IVDU, Dental infection, artificial valve and any implanted devices.

113
Q

Post Arrest Care and post arrest targets

A
  1. Identify cause
  2. Neurocritical care
  3. Shock MGMT
  4. Ischemia/reperfusion
114
Q

Discuss IABP and how it works

A

The IABP consists of a balloon catheter, which is typically inserted percutaneously into the femoral artery and advanced into the descending thoracic aorta, and a pump that controls inflation/deflation.

**The balloon is inflated as diastole beings, augmenting aortic pressure and thus coronary perfusion during the diastolic period. During systole the balloon is deflated and help augment the pull of fluid from the ventricle, decreasing afterload.

115
Q

Hypovolemia causes

A

Diarrhea, dehydration, diuresis, hemorrhage

116
Q

Three top tips for pharmacology

A

1) if your liver or kidneys are fucked, your drug handling will be also
2) Its better to give too little and have to give additional than other way around
3) whenever you give a drug, you give its effect and side effect

117
Q

Ketamine, go.

A

NMDA antagonism, dissociated anesthesia.

  • Induction 1-2mg/kg
  • augments opiates
  • sedation/induction
  • cardio-stable but still has those negative effects
  • unstable patient 1mg/kg
  • delirium, augment with midaz
  • bronchodilation
  • hypersalvation
  • not appropriate for ACS
118
Q

Mysthesia Gravis definition

A

MG is an acquired autoimmune disorder of the neuromuscular junction characterized by weakness of skeletal muscles, proximal weakness.

119
Q

when do you intubate a MG patient

A

-< 20ml/kg

120
Q

Myasthenia Gravis Patho

A

immunoglobulin autoantibodies play a pathogenically important role by attaching ACh receptors and reducing the number of Ach receptors over time, therefore unable to depolarize muscles

121
Q

Guillain-Barre Syndrome

A

Acute demyelinating disease.
-Exposure to make antibodies (GI, UTI, PNA) to fight off pathogen, but antibodies cross react with myelin and destroy myelin in the major peripheral nerves because of that nerves weather away and you get weak and decreases saltatory conduction. Starts peripherally at first, then centrally.

Miller Fisher = GBS with Cranial nerve involvement

122
Q

GBS tx

A

IV IG, plasma exchange

123
Q

MG tx

A

IV IG, Plasma Exchange + steroids

124
Q

Pulsus paradoxus patho

A

i. During normal spontaneous breathing, inspiration causes blood to fill the RA from the vena cava and causes increased RV filling with a slight bulge or ventricular septum into the LV
ii. This causes a small decrease in LV ejection with systole (increased afterload/decreased LVEDV). In normal breathing, SBP can normal fall on spiration by 10mmHg
iii. Pulsus Paradoxus is an exaggeration of this normal BP variation with breathing. It is defined as a fall in SBP by more than 10mmHg during spontaneous inspiration.
In mechanically ventilated patients, a reversal of this pressure variation occurs, PPV displaces the LV wall inward during systole to assist in LV emptying. This causes a slight rise in SBP during mechanical inspiration.

125
Q

HCM ECG

A
  1. large dagger-like “septal Q waves” in the lateral — and sometimes inferior — leads
  2. LVH due to the abnormally hypertrophied interventricular septum
126
Q

cardiac axis deviated to left and causes

A

too much LV muscle 💪 or bad right sided infarct💔

  • lead 1 is more positive and aVF is negative
127
Q

extreme right cardiac deviation

A

think metabolic or tox, like TCA.

-negative in both

128
Q

Alteplase name and IV regimen

A

t-PA. Bolus + infusion (usually for CVA - must be given within 4.5 hours, but aim for within 3 hours)

129
Q

Tenecteplace name and IV regimen

A

TNK. 1x Bolus, weight based max 50mg

130
Q

Preferred P2Y12 and dose

A

Ticagrelor 180mg

131
Q

Plavix dose for STEMI

132
Q

Infectious endocarditis causes

A

IVDU, dental infections, artificial valve replacement and anything impacted

133
Q

infective endocarditis tx

A

prolonged ABX, typically won’t replace valve unless refractory HF or size of vegation meets criteria

134
Q

aortic aneurysm complications

A

-rupture, aortic regurgitation, tracheal or esophageal compression, pulmonary artery outflow obstruction, septic embolism

a-aortic insufficiency
o-occlusion of coronary arteries
r-rupture
t-tamponade
i.=ischemia of viscera
c=cva
135
Q

Aortic dissection BP targets

A

100-120mmHg, HR 55-60 - think labetalol

136
Q

DVT prophylaxis contraindications

A

Post brain bleed, HIT (heparin induced thrombocytopenia) and recent neurosurgery

137
Q

Severe acute hypertension tx

A

PO = clonidine
IV = hydralzine/labetalol
carefully ~25% below presenting BP within 24 hours
SBP >180,DBP >120

138
Q

Pacing position 1

A

chamber being paced

139
Q

Transvenous box has

A

sensitivity, voltage, and rate

140
Q

Pacing position 2

A

chamber being sensed

141
Q

Pacing position 3

A

response to sensing

142
Q

VVI =

A

Ventricular pacing and seeing (temporary)

143
Q

DDD =

A

Pacing and sensing the atria and ventricular (most common)

-Permanent DDD

144
Q

Ductus Arteriosus

A

By pass pulmonary circulation (connects pulmonary artery and aorta)

145
Q

Ductus Venous

A

In the liver circulation, between the umbilical vein and IVC

146
Q

Patent Foramen Ovale

A

Shunt from the atrium right to left, prostaglandin releases causes it to close.
Smaller shunt opening that is essentially a valve, because during fetal circulation, blood travels to the right to left in the Atrium, and then after delivery, when breathing starts, PFO essentially closes because pressure in the LA keeps the valve shut essentially

147
Q

Eisenmenger Syndrome

A

□ ASD/VSD increases PA pressure with left to right shut
□ Overtime, PVR increases resulting in bidirection flow
Pulmonary Vascular Resistance increases, shunt reverse Right - to - Left –> Eisenmenger syndrome.

148
Q

Post arrest Care steps

A
  1. Identify cause and history
  2. Neurocritical care
  3. Shock MGMT
  4. Ischemia/reperfusion
149
Q

NAGMA causes and tx

A

Hyperchlorermia, RTA, GI losses = treated with HCO3-

150
Q

Metabolic alkalosis subcategory and tx

A
  1. Volume (Cl) responsive
    - tx with NaCl.
    - Chloride will bind with H+ and Na+ with Hco3- and drop pH
  2. non-volume response = malignant causes usually, long term non CCP tx
151
Q

Normal hemodynamics: SvO2,CO, SV, SVR, CVP, PAWP

A

SvO2 70%

CO 4-8L/m

SV 60-100mL/beat

SVR 800-1200

CVP 2-6mmHg

PAWP 6-12mmHg

152
Q

Hard signs of neck injuries

A
  • expanding hematoma
  • severe active bleeding
  • shock not responding to fluid
  • decrease or absent radial pulse
  • vascular bruits/thrills
  • cerebral ischemia
  • airway obstruction
153
Q

Soft sign of neck injuries

A
  • hemoptysis, hematemesis
  • oropharyngeal blood
  • dyspnea
  • dysphonia, dysphagia
  • subcutaneous or mediastinal air
  • chest tube air leak
  • nonexpanding hematoma
  • focal neurologic deficits
154
Q

zones of the neck

A 
Zone 1
○ Clavicle to cricoid cartilage 
Zone 2
○ Cricoid cartilage of angle of mandible
 Zone 3
   - Angle of the mandible to base of the skull
155
Q

Hemostasis 5 stages

A
  1. vasoconstriction
  2. primary hemostasis - platelet plug
  3. secondary hemostasis - coagulation
  4. fibrinolysis - dissolves the clots, restores function
  5. regeneration - repair
156
Q

Ectopic pregnancy definition and most common clinical presentation

A

An ectopic pregnancy is an extrauterine pregnancy. Almost all pregnancies occur in the Fallopian tube.
the most common clinical presentation of ectopic pregnancy is first-trimester vaginal bleeding and/or abdominal pain

157
Q

Ruptured ectopic pregnancy definition and presentation

A

If there is a rupture of and hemorrhage from the structure in which the pregnancy is implanted, usually the Fallopian tube, patients can become hemodynamically unstable.

Sudden onset of severe and persistent abdominal pain, syncope and hemodyanic instability. Clinical dx made primarily on finding of echogenic fluid in the pelvic cul-de-sac during POCUS

158
Q

Ruptured AAA tx

A

Dissection SBP <120-100mmHg with HR 55-60

Actually rupture is a surgical emergency, end-vascular or open repair of the rupture. High mortality.

159
Q

AAA rupture presentation

A

Dead.

Ruptured AAA is uniformly fatal, with death occurring within hours. Hemodyncamilly unstable patients with known AAA who present with classic symptoms (hypotension/backpn/pulsatile mass) should be taken directly to the OR for immediate control of hemorrhage and repaid of the aneurysm.

160
Q

Mesenteric Ischemia definition

A

Ischemia affecting the small intestine is generally referred to as mesenteric ischemia.

161
Q

Mesenteric ischemia patho

A

Occlusive arterial obstruction is due to acute embolism or thrombosis and most commonly affects the superior mesenteric artery

Venous thrombosis is due obstruction of the intestinal outflow tract, including the superior and inferior mesenteric veins and splenic and portal veins.

Non-occlusive mesenteric ischemia is a result of low-flow state and is most commonly due to vasoconstriction from low-cardiac output or the use of vasopressors

162
Q

Bowel obstruction definition

A

bowel obstruction occurs when the normal flow of intraluminal contents is interrupted. either functional obstruction or mechanical

163
Q

Bowel obstruction patho

A

Mechanical obstruction is caused by either intrinsic luminal obstruction or extrinsic compression of the small bowel - hernias, malignancies, and infective/inflammatory disorders

  • Obstruction leads to progressive dilation of
  • The bowel will become edematous, normal absorptive function is lost and fluid is sequestered into the bowel lumen. Then ischemic necrosis of the bowel is most commonly caused by twisting of the bowel
164
Q

pancreatitis definition

A

Acute pancreatitis is an inflammatory condition of the pancreases by enzyme-mediated auto digestion

165
Q

Pancreatitis patho

A

The bile duct from the gallbladder and liver connects to the pancreatic duct, which connects to the duodenum. Normally, the pancreas releases exocrine digestive enzymes into the intestine. In acute pancreatitis the inflammation damages and destroys the pancreatic cells and digestive enzymes are released in the pancreas itself and not into the duct, damaging tissue and vasculature. ++ lipase in the blood

166
Q

pancreatitis etiologies - GETSMASHED

A 
Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune
Scorpion venom 
Hypercalcemia/lipidemia
ERCP
Drugs
167
Q

SAH 6 complications

A
  1. rebreeding
  2. seizures
  3. hydrocephalus
  4. arrhythmia
  5. Na+ disorders (CSW, SIADH, DI)
  6. Vasospasm
168
Q

Cerebral salt wasting patho

A

CSW is characterized by hyponatremia and ECF depletion due to inappropriate sodium wasting in the urine. occurs due to hypothalamus and

169
Q

SIADH defintion

A

the SIADH is a disorder of impaired water excretion caused by the inability to suppress the secretion of ADH

170
Q

SIADH patho

A

often involves the hypothalamus. ADH secretion results in a concentrated urine and therefore a reduced urine volume. This leads to water retention, which increased TBW, which lowers plasma concentration by dilution.

171
Q

SIADH Tx

A

HTS 3% 50-100ml/Hr

172
Q

UGIB definition, patho and causes

A

UGIB - any bleeding proximal to ligament of Treitz. BUN:Cr ratio >30 suggests UGIB.

presents with hematemesis (vomiting blood or coffee-ground like emesis and/or melon)

173
Q

UGIB Treatment

A

ABCs etc, type and screen, avoid intubation as possible to allow for resuscitation first.

  • transfuse 1:1:1, reverse coagulopathies
  • give PPI
  • give octreotide (25mcg bolus then 25-50mcg/hr)
  • balloon tamponade
174
Q

LGIB

A

Bleeding distal to ligament of Treitz

-acute lower GI bleeding refers to blood

175
Q

LGIB causes

A

diverticular disease, vascular extasia, mesenteric ischemia, mocker’s diverticulum

176
Q

CSW tx

A

HTS 3% 50-100cc and fludrocortisone 0.1-0.3mg/daily

177
Q

DI definition

A

Diabetes inspidus is characterized by decreased release of ADH resulting in variable degree of polyuria

178
Q

Diabetes Inspidius patho

A

occurs with damage to hypothalamus and decreased ADH production, results in increased sodium and polyuria

179
Q

DI Tx

A

replace ADH with DDAVP 2mcg q 12 hours or vasopressin 0.03units/min

180
Q

acute kidney injury definition

A

AKI is an abrupt and usually reversible decline in GFR. This results in an elevation of serum blood urea nitrogen (BUN), creatinine, and other metabolic waste products thet are normally excreted by the kidney

181
Q

patho of AKI, pre/intra/post renal injury

A

Pre-renal: decreased perfusion of normal kidney, hypovolemia, poor cardiac output, renal artery and small vessel disease.

Intra-renal: Glomerular injury - glomerulonephritis (nephrotic syndrome), tubular - acute tubular necrosis, interstitial disease and vasculitis.

Post-renal injury: obstruction to urinary outflow, ureter - renal stone, urethras and bladder outlet - prostate enlargement

182
Q

AKI RF

A

Meds - NSAIDS, ACE-I, ARBs,

Drugs - cocaine, etoh,

Contrasts - iodinated contrast

systemic disease - gout, HTN, CAD, sepsis, hepatic disease, malignancy

183
Q

AKI mgmt summary

A

1) ID patients who need to go for urgent RRT
a) hypervolemia with pulmonary edema
b) severe hyperkalemia
c) life-threatening ureic syndrome
d) toxic exposure

2) volume assessment and mgmt
3) manage electrolytes and balances
4) manage acid-base disturbances
5) hemodialysis indications

184
Q

Hemodialysis indication

A
  • refractory hyperK
  • refractory hypo/hypernatremia
  • hypervolemia with pulmonary edema
  • uremia with pericarditis/seziures
  • refractory acidosis (<7.1)
  • dialyzable toxins - lithium, asa, methanol, ethylene glycol,
185
Q

kidney damage is identified by

A

presence of albuminuria

186
Q

decreased kidney function is ID by

A

eGFR < 60mL/min

187
Q

general difference between HHS from DKA

A

they are differentiated by absence of ketoacidosis and degree of hyperglycaemia.

188
Q

DKA pathophysiology

A
  1. The damaged pancreas results in a decrease production of insulin, this creates an increase in gluconeogenesis, and decrease in glycolysis, resulting in hyperglycaemia creating polyuria, polydipsia and glucosuria.
  2. Theres also an increase in lipolysis, which creates free fatty acids that go to the liver and undergo ketogenesis, which produces more ketones resulting in hyperketonemia. Ketones are acidic, resulting in pH drop.
189
Q

DKA definition

A

is characterized by the triad of hyperglycaemia, anion gap metabolic acidosis and ketonemia.

190
Q

DKA aetiologies (5 I’s)

A
  1. infection
  2. intoxication
  3. infarction
  4. inappropriate withdrawal from insulin
  5. intercurrent illness
191
Q

HHS Definition

A

Progressive hyperglycaemia and hyperosmolarity in patients with poorly controlled T2DM and limited access to water and commonly a precipitating illness

192
Q

HHS pathophysiology

A

Progressive hyperglycaemia and hyperosmolarility in patients with poorly controlled T2DM

Three main factors:

  1. insulin resistance
  2. inflammatory state with pro inflammatory cytokines resulting in increased hepatic glugoneogesis and glycogenolysis
  3. osmotic diuresis and renal excretion of glucose

Because of hyperglycaemia, water is pulled into the intravascular compartment. Kidneys aren’t able to reabsorb this much glucose, so a lot of glucose is lost in the urine where water continues to follow (polyuria).

  • Creating a loss of intravascular volume and high concentration of osmotically-active solutes (hyperosmolarity)
  • T2DM insulin that’s present inhibits keto genesis pathway
193
Q

tPA MOA

A

Tissue plasminogen activator converts plasminogen to plasmin which breaks down cross-linked fibrin to several fibrin degradation products

194
Q

Phases of hemostasis

A
  1. vasoconstriction
  2. primary hemostasis - platelet aggergation
  3. secondary hemostasis - coagulation cascade
  4. fibrinolysis
  5. regeneration
195
Q

Activated Partial thromboplastin time (aPTT)

A

is used to assess deficiencies or inhibitors of the intrinsic pathway factors and common pathway factors

196
Q

Anti-Xa assay are used to measure

A

the anticoagulation activity of an anticoagulant that inhibits clotting factor Xa such as heparin, LMWH, and fondaparinux

197
Q

INR international normalized ratio

A

INR= PT/mean normal PT

198
Q

Prothrombin Time

A

the PT is used to assess deficiencies or inhibitors of the extrinsic pathways

199
Q

D-dimer

A

are breakdown products generated by the action of plasmin on cross-linked fibrin

200
Q

APAP overdose pathophysiology

A

• Pathophysiology:
○ Tylenol is metabolized 97% by glucuronidation, sulfation and 3% by CYP450.
○ The CYP450 converts Tylenol into NAPQI, which is broken down by glutathione into non-toxic metabolites.
○ During Tylenol OD, Glutathione levels get depleting leaving high levels of NAPQI.
○ NAPQI are hepatotoxic resulting in liver damage
The nomogram is used to direct decision on time and APAP levels for NAC treatment.

201
Q

Tylenol metabolism

A 
○ Glucuronidation
		○ Sulfation
		○ CYP450 + Glutathione
		○ Unchanged
			§ NAPQI created cellular toxicity 
			§ NAPQI builds up and results in hepatic necrosis
NAPQI is the cause for APAP toxicity
202
Q

principle of therapy for Tylenol

A 
○ NAC (N-acetylcysteine)
			§ Enhances sulfation
			§ Glutathione precursor
			§ Glutathione substrate
Free radial scavenger and antioxidant
203
Q

Hypernatremia fluid replacement equation

A

Desired water replacement in first day in ml = 3ml/kg bodyweight x 10 (then divide by 24 to get hourly rate; and add the additional water losses)

204
Q

how do you manipulate Flow (vCalc)

A

product of Vt and iTime

205
Q

How do you adjust PIP

A

I-Time, and decrease flow (Vt) and decrease resistance

206
Q

liver cirrhosis patho

A

An increase in intrahepatic vascular resistance due to architectural distension and deficiency of NO

207
Q

Varices patho

A

Varices develop from the esophagus and stomach dilation of preexciting vessels and active angiogenesis. They increase in size with the severity of portal HTN and can rupture with bleeding when the pressure exceeds a maximal portion

208
Q

Portal HTN

A

results from combination of increased intrahepatic resistance and splanchic arterial vasodilation.

209
Q

varices medical mgmt

A

vasopressin, octerotide, blood, Blakemore

210
Q

Surviving sepsis campaign advocates for one hour bundle that focuses on protocolized care that includes the following:

A
  • obtain lactate levels
  • get cultures
  • source control
  • start broad spectrum empiric antibiotics
  • give 30cc/kg fluid bolus for hypotension or lactate >4
  • start vasopressors if MAP remains <65 during or after fluid bolus
211
Q

Sepsis definition

A

○ Life-threatening organ dysfunction caused by a dysregulated host responsive to infection
Organ dysfunction defined as an increase of two or more points in the SOFA score

212
Q

Septic shock

A
  • Fullfill the criteria for sepsis

- despite adequate fluid-resuscitation requires vasopressors to maintain a MAP >65 and a lactate > 2

213
Q

Simple heart failure definition

A

inability of the heart to meet the metabolic demands of the body at normal ventricular filling pressures, implies impaired function

214
Q

Simple definition of cardiomyopathy

A

Refers to a group of disease of the heart muscle. Implies altered structure.

215
Q

Urine Alkalinization

A

Ion trapping

Acids are ionized in alkaline environment

CCP - Semester 2 (14 decks)

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