Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Boards Review > General Review > Flashcards

General Review Flashcards

1
Q

Antigen presenting cells:

A

macrophages
B-lymphocytes
Dendritic cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

T-cells:

A

T cytotoxic: killer T-cells

T helper cells:
T helper 1
T helper 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

T cytotoxic cells action.

A

killer T-cells, recognize MHC 1 = intracellular antigens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

T helper cells general actions.

A

recognize MHC 2 on APCs → activate other cells. APC’s are not infected.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

T helper 1 cells action.

A

activate macrophages, natural killer cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

T helper 2 cells action.

A

activate B-cells → Ab production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Complement pathways

A

Classical
Lectin
Alternative pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Classical complement pathway is activated by:

A

Ag-Ab complexes or acute phase proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Lectin complement pathway is activated by:

A

mannose binding protein (MBP) binding to Antigen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Alternative complement pathway is activated by:

A

foreign pathogens without antibody

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Endpoint of complement pathways:

A

All 3 pathways end the same…

  • Enhanced attachment or opsonization (C3b)
  • Trigger inflammation/phagocyte chemotaxis (C5a)
  • MAC → cell lysis (C5b and others)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Immunoglobulin structure- draw

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Hypersensitivity reactions with examples:

A

Type 1: IgE mediated → eosinophils → anaphylaxis.
Ex: bee sting

Type 2: cytotoxic. Complement mediated or Ab mediated → cell or receptor destruction.
Ex: IMHA, transfusion reaction, myasthenia

Type 3: Ag-Ab complex deposition.
Ex: lupus, lyme GN

Type 4: Delayed: T-cell mediated with prior sensitization → Macrophage activation.
Ex: albumin rxn

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

List the Endognous pyrogens and their effects:

A

IL 1
IL 6
TNF-a.

→ cytokine release, macrophage stimulation, release of prostaglandin → hypothalamus → raise set point

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Define SIRS & nSIRS

A

Systemic inflammation.

nSIRS = non-infectious

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Define sepsis (OLD)

A

SIRS due to an infection.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Define sepsis (NEW)

A
  • life-threatening organ dysfunction caused by a dysregulated host response to infection.
  • Acute change in SOFA score >/= 2 from baseline (assumed 0 if previously healthy)
  • qSOFA: RR > 22, Systolic BP < 100, altered mentation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Define severe sepsis (OLD)

A
  • OLD definition, eliminated with sepsis 3.
  • Sepsis + organ dysfunction, hypotension, or impaired perfusion.
  • In sepsis 3, all sepsis is “severe”.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Define Septic Shock (OLD)

A

severe sepsis with hypotension requiring pressors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Define Septic Shock (NEW)

A
  • Subset of sepsis in which underlying circulatory and cellular/metabolic abnormalities are profound enough to substantially increase mortality.
  • Requires pressors to maintain systolic BP > 65
  • Lactate > 2 despite adequate volume resuscitation
  • Hospitality rate > 40%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Define MODS (OLD)

A

sepsis or SIRS + 2 or more organ dysfunctions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Define MODS (NEW)

A
  • Any acute change in total Sequential Organ Failure Assessment (SOFA) score >/= 2 points as a result of sepsis or nSIRS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

SIRS criteria (cat)

A

3 or more

  • T < 100 or > 103.5
  • HR < 140 or > 225
  • RR > 40
  • WBC < 5K or > 19.5K
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

SIRS criteria (dog)

A

2 or more

  • T < 100.6 or > 102.6
  • HR > 120
  • RR > 20
  • WBC < 6K or > 16K or 3% bands
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Endpoints of goal directed therapy (old stuff…)

A
  • Macrocirculation: CVP 7-10, MAP > 65, UOP > 0.5ml/kg/hr
  • Microcirculation: Lactate < 2.5, ScvO2 > 70
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Inflammatory Cytokines in sepsis:

A

IL 1
IL 6
IL 8 (aka CXCL8)
IL 12
TNF-a.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Anti-Inflammatory Cytokines in sepsis:

A

IL 4
IL 10
TGF-b

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Mechanisms of vasodilation in sepsis:

A
  • Activation of ATP-K channels in smooth muscle due to inflammation → prevention of Ca influx
  • Increase nitric oxide release
  • Vasopressin depletion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Mechanisms of septic myocardial dysfunction:

A
  • Global ischemia
  • Unknown circulating myocardia depressant factor
  • Cytokines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Mechanisms of hypocalcemia in critical patients

A
  • Increased calciuresis
  • Dilution
  • Cellular uptake due to muscle damage
  • Chelation with citrate or lactate
  • Altered hormones (PTH, vit D)
  • Saponificaiton of fat (pancreatitis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Positive Acute phase proteins:

A
  • mannose binding protein
  • fibrinogen
  • haptaglobin
  • C-reactive protein
  • Serum Amyloid A
  • Ceruloplasmin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Negative Acute phase proteins:

A
  • albumin
  • antithrombin
  • transferrin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Definitions of nosocomial infection: infection that is first diagnosed….

A
  • > 48 hrs after admission
  • Within 2 weeks of hospitalization
  • After transfer from another facility
  • < 30 days post op
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Mechanisms of bacterial resistance transfer:

A

Transformation: pick up naked DNA laying around

Transduction: bacteriophage (virus) transfers DNA

Conjugation: plasmid transferred by bacterial “sex”. #1 method

Random mutation → Natural selection/replication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Briefly explain transformation in terms of bacterial resistance.

A

pick up naked DNA laying around

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Briefly explain transduction in terms of bacterial resistance.

A

bacteriophage (virus) transfers DNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Briefly explain transduction in terms of bacterial resistance.

A

plasmid transferred by bacterial “sex”. #1 method

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Lab findings in tumor lysis syndrome:

A

hyperphosphatemia
hypocalcemia
increased uric acid
azotemia
hyperkalemia
metabolic acidosis
multiple organ failure
shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Mechanisms of heat loss:

A

Radiation
Conduction
Convection
Evaporation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Briefly explain radiation as a mechanism of heat loss.

A

exchange b/w objects and environment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Briefly explain conduction as a mechanism of heat loss.

A

objects in direct contact

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Briefly explain convection as a mechanism of heat loss.

A

movement of fluid or air over body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Briefly explain evaporation as a mechanism of heat loss.

A

heat energy turns liquid → gas (ie sweat)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Classification of surgical wounds:

A

Clean
Clean-contaminated
Contaminated
Dirty

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Briefly explain a clean-contaminated surgical wound.

A

entered a lumen and kept it clean

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Briefly explain a contaminated surgical wound.

A

overt leakage/contamination at sx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Briefly explain a dirty surgical wound.

A

already infected/contaminated prior to sx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

RER=

A

RER= (30 x kg) + 70 = 70 kg^0.75

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

TPN calculations:

A

Protein: 4kcal/g
(Dog: 4-5g/100kcal, Cat: 6-8g/100kcal)

Dextrose: 30-50% of remaining Kcal.
50% dextrose = 1.7kcal/ml

Lipid: 50-70% of remaining Kcal.
20% lipid = 2kcal/ml

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Anterior Pituitary sections:

A

Makes TSH
ACTH
LSH
FSH
prolactin
GH (not stored really)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Posterior Pituitary sections:

A

Stores and releases ADH/vasopressin and oxytocin (these are made in magnocellular neurons of the hypothalamus)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Transudate classification & examples

A

TP < 2.5, < 1000 cells/µL.

Low alb, portal hypertension, vasculitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Modified Transudate classification & examples

A

TP > 2.5, 1000-5000 cells/µL.

CHF, vasculitis, lymph obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Exudate classification & examples

A

TP > 2.5, > 5000 cells/µL.

Blood, chyle, suppurative, septic, neoplastic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Abdominal effusion chemistry ratios:

Uroabdomen

A

Creat > 2 abdomen : 1 peripheral

K > 1.4 abdomen : 1 peripheral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Abdominal effusion chemistry ratios:

Bile peritonitis

A

Bili > 1.2 abdomen : 1 peripheral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Septic abdomen

A

Abd glu > 20 less than serum

Abd lactate 2 x more than serum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

A-Fast views:

A

Ideally R lateral recumbency
DH view (diaphragmaticohepatic)
Splenorenal (L)
Cystocolic
Hepatorenal (R)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

T-Fast views:

A

R and L chest tube sites: probe horizontally, look for pneumo

R and L pericardial sites: probe both ways and scan, look for fluid, heart

DH view: pericardial effusion, ab effusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Adrenal gland layers:

A

Medulla: Norepi (cat), epi (dog)

Cortex:
- Zona glomerulosa: outer, salt (mineralocorticoids)
- Zona fasciculata: middle, sugar (glucocorticoids)
- Zona reticularis: inner, sex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Zona glomerulosa:

A

outer, salt (mineralocorticoids)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Zona fasciculata

A

middle, sugar (glucocorticoids)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Zona reticularis

A

inner, sex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Renin-AT-Aldosterone system:

A

Angiotensinogen (from liver) →(via renin from JG cells) → AT I → (via ACE from lung) → AT II

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

AT II effects:

A
  • Na reabsorption → H20 Reabsorption
  • Vasoconstriction
  • Sympathetic stimulation → Increased RH/inotropy, vasoconstriction
  • Aldosterone release → H2O/Na retention
  • ADH → H20 reabsorption and vasoconstriction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Phase 1 metabolism reactions:

A

oxidative
reductive
hydrolytic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Phase 2 metabolism reactions:

A

conjugation
(glucaronic acid, sulfate, glutathione, acetylation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Causes of ascites in liver disease:

A
  • Portal hypertension
  • Splanchnic vasodilation
  • RAAS sodium retention
  • Hypoalbuminemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Causes of PU/PD in liver disease:

A
  • Encephalopathy
  • RAAS sodium retention
  • Medullary washout (no urea)
  • Increased endogenous steroids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Hepatic encephalopathy mediators:

A
  • ammonia
  • manganese
  • glutamate/glutamine
  • GI toxins
  • increased GABA
  • endogenous benzos
  • aromatic AAs
  • Mercaptans
  • Skatoles
  • Indoles
  • Bile acids
  • Serotonin
  • Phenol
  • Tryptophan
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Path of bile flow:

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Cranial nerves:

A
  1. Olfactory
  2. Optic (vision)
  3. Oculomotor (PLR and most motor)
  4. Trochlear (dorsal oblique)
  5. Trigeminal
    (a) Ophthalmic (sensory eye)
    (b) Maxillary (sensory teeth)
    (c) Mandibular (masticatory mm, tongue sensory)
  6. Abducent (lateral rectus, retractor bulbi)
  7. Facial (face motor, tongue sensory)
  8. Vestibulocochlear (vestibular, hearing)
  9. Glossopharyngeal (swallowing, tongue taste)
  10. Vagus (parasympathetic)
  11. Accessory (neck mm)
  12. Hypoglossal (tongue motor and swallowing)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Modified Glasgow Coma Scale

A
  • Level of consciousness (0-6)
  • Brain stem reflexes (0-6)
  • Motor reflexes (0-6)
  • Total score 0-18 (higher is better)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Mechanisms of secondary brain injury

A
  • Increased excitatory neurotransmitters (glutamate) → ATP depletion
  • Ca/Na entry into cells (pumps fail) → swelling (cytotoxic edema)
  • ROS → peroxidation injury
  • Bleeding → iron → worse ROS
  • Increased vascular permeability (leaky BBB) → vasogenic edema
  • Loss of pressure autoregulation due to NO induction
  • Increased ICP → ischemia → worsened injury
  • Systemic hypotension or hypoxia → ischemia → worsened injury
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Hind end nerve roots

A

Femoral: L4-6 (Patellar and hip flexors)
Sciatic: L6-S2 (withdrawal)
Pudendal: S1-3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

CVP waveform: be able to draw, label, explain all parts.

A

A wave = RA contraction (highest pressure)

C wave = Bulging of TV into RA (early RV systole)

X descent= RV emptying

V wave= rapid atrial filling (TV closed)

Y descent= TV opens, ventricular filling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Capnogram: be able to draw, label, explain all parts (normal and some common abnormals)

A

A-B = phase 1 = dead space exhalation

B-C = phase 2 = intermediate airways

C-D = phase 3 = alveolar gas

D = ET CO2

D-E= inhalation

Abnormals: Curare cleft, obstruction to exhalation, rebreathing, death/severe hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Draw curare cleft capnograph waveform

A

Breakthrough breathing during IPPV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Draw obstruction to exhalation capnograph waveform

A

Obstruction in expiratory limb of circuit

Also, Bronchospasms/Asthma, COPD, upper airway FB, partially kinked or occluded airway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Draw a rebreathing capnograph waveform

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Draw a death/severe hyoptension capnograph waveform

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Draw a hypoventilation capnograph waveform

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Draw a hyperventilation capnograph waveform

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Draw:
Flow volume loop normal

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Draw:
Flow volume loop abnormal -jagged

A

Airway secretions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Draw:
Flow volume loop abnormal - scooped

A

small or medium airway obstructions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Draw:
Pressure volume loop normal

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Draw:
Pressure volume loop normal - decreased compliance

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Draw:
Pressure volume loop normal - changes in resistance

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Draw:
Pressure volume loop normal - Leak

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Draw:
Flow-time scalars with both volume and pressure controlled ventilation

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Draw:
Pressure-time scalars with both volume and pressure controlled ventilation

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Draw:
Volume-time scalars with both volume and pressure controlled ventilation

A
94
Q

Compliance

A

Compliance = 𝝙V/𝝙P

95
Q

Elastance

A

Elastance = 𝝙P/𝝙V

96
Q

Haldane effect

A

O2 offloading → increased CO2 affinity

97
Q

Bohr effect:

A

increased CO2 (acidosis) → decreased O2 affinity

98
Q

PaO2/FiO2 ratio:

A

PaO2 should be 5x FiO2 (or PaO2/FiO2 as a decimal = 500)

99
Q

Residual volume

A

= volume left in lungs after max expiration

100
Q

Total lung capacity

A

= volume in lungs after maximal inspiration (everything)

101
Q

Tidal volume

A

= normal volume of inspiration

102
Q

Expiratory reserve volume

A

= extra amount you can expire (still can’t ever get RV)

103
Q

Inspiratory reserve volume

A

= extra amount you can inspire

104
Q

Functional residual capacity

A

= volume left in lungs after normal expiration = RV + ERV

105
Q

Inspiratory capacity

A

= maximum amount you can inspire= TLC - FRC = IRV + TV

106
Q

Vital capacity

A

= total moveable air, air expired after a maximal insp/exp = TLC - RV

107
Q

Airway pressure during inspiration:

A

𝝙P = 𝝙TV/ compliance + (Resistance x 𝝙Flow)

108
Q

O2 saturation left curve shifts:

A

= increased affinity

=
alkaline
cold
decreased 2,3 DPG (fetus)
CO

109
Q

O2 saturation right curve shifts:

A

= decreased affinity = increased offloading

=
high (increased 2,3 DPG)
hot
acid

110
Q

Fick’s law of gas diffusion:

A

Volume of gas/time = Area/thickness x diffusion constant x 𝝙PP

𝝙PP = partial pressure difference

Diffusion constant = solubility/ √MW

111
Q

Equation of motion (ventilator):

A

pressure = (TV/compliance) + (resistance x flow)

112
Q

A-a gradient

A

= PAO2 - PaO2

PAO2 = FiO2 decimal x (barometric pressure - 50) - (PaCO2 x 1.1)

Barometric pressure at sea level = 760

50 = water pressure

PaO2 comes from your blood gas

Normal A-a gradient = < 15

113
Q

Causes of hypoxemia:

A
  1. decreased FiO2
  2. hypoventilation
  3. diffusion impairment
  4. V/Q mismatch
  5. shunt (severe V/Q mismatch)
114
Q

Causes of tissue hypoxia:

A

PA pressure = 4 x TR2

115
Q

PHT pathophysiologic causes (3):

A
  1. Increased pulmonary vascular resistance: vasoconstriction, occlusion, remodeling (chronic lung disease), polycythemia
  2. Increased blood flow (L → R shunt)
  3. Increased LA pressure (MR)
116
Q

PHT categories based on new consensus statement?

A

— need answer

117
Q

What are the ARDS/ALI Criteria:

A
  • Acute onset
  • No evidence of cardiac dysfunction (based on echo, heart size on rad, or PCWP < 18)
  • Pulmonary infiltrate with high protein fluid
  • Hypoxemia: PF ratio 300-200 is mild, 200-100 is moderate, < 100 is severe- all with 5 PEEP
  • Risk factors (ie systemic inflammation)
118
Q

Fill in this chart:
NEED STATISTICS CHART

A
119
Q

Define Sensitivity.

A

= ability to correctly ID those with disease

= true pos / all disease pos

= true pos/(true pos + false neg)

120
Q

Define Specificity

A

= ability to correctly ID those without disease

= true neg / all disease neg

= true neg/(true neg + false pos)

121
Q

Define Positive predictive value

A

= likelihood that patient has a disease with a positive result

= true pos / all test pos

= true pos/(true pos + false pos)

122
Q

Define Negative predictive value

A

= likelihood that patient doesn’t have a disease with a negative result

= true neg / all test neg

= true neg/(true neg + false neg)

123
Q

Define accuracy.

A

= # correct tests/all tests

= (TP + TN)/(TP + FP + TN + FN)
Accuracy = [sensitivity (prevalence)] + [specificity (1- prevalence)]

124
Q

Define Likelihood ratio

A

= how much more likely it is that a patient with a positive test has a disease compared to a patient with a negative test

= sensitivity/ (1-specificity)

125
Q

CO equation & normals

A

= SV x HR

normal = 100-200 ml/kg/min

126
Q

CI equation

A

= CO/body surface area in m2

127
Q

O2 Deliver equation

A

DO2 = CO x CaO2

128
Q

Arterial O2 content equation

A

CaO2 = (1.3 x SaO2 x Hb) + (PaO2 x 0.003)

= bound + unbound

129
Q

O2 consumption equation

A

VO2 = CO x (CaO2 - CvO2)

130
Q

Oxygen extraction ratio equation & normal

A

OER = VO2/DO2

= (SaO2-SvO2)/SaO2.

Normal = 25%
Higher = inadequate O2 delivery

131
Q

Systemic vascular resistance equation

A

= (MAP - CVP) / CO

132
Q

Fick principle equation (to calculate CO):

A

CO = VO2/(CaO2 - CvO2)

133
Q

Normal heart pressures:

A
  • RA mean 0-5
  • RV 25/5
  • PA 25/10
  • LA mean 5-10
  • LV 125/10
  • Aorta 125/80
134
Q

Cerebral perfusion pressure equation

A

= MAP - ICP

135
Q

Coronary perfusion pressure equation

A

= Diastolic aortic pressure - RA pressure

136
Q

Law of LaPlace (Wall tension) equation

A

Tension = pressure x radius/wall thickness

(I do not really understand where this applies)

137
Q

Pouisselle’s Law equation

A

Flow = (𝛑 x 𝝙 P x r4)/8nL

n= viscosity
Flow = 𝝙 P/ resistance

138
Q

Ohm’s law equation

A

= rearranged Pouiselle’s

= Pressure = blood flow x resistance

139
Q

Starling’s Law equation:

A

Net filtration (OUT of vessel) = Kf [(Pcap - Pint) - 𝛔 (𝛑cap - 𝛑int)

Kf = permeability
𝛔 = reflection coefficient

140
Q

Explain how to set up and test a direct arterial BP system. — NEED TO WRITE OUT ANSWER

A
141
Q

Arterial system dampening:

Ideal

A

Ideal: 2-3 oscillations after the square wave, each drop by ⅔ to the next one

142
Q

Arterial system dampening:

Overdamped

A

Too few oscillations, too flat

Compliant tubing, air in tubing, clot in catheter or tubing, narrow tubing

143
Q

Arterial system dampening:

Underdamped

A

Too many oscillations, doesn’t drop enough

Stiff tubing, tachycardia or dysrhythmia, long tubing

144
Q

Albumin deficit (in grams) equation:

A

= 3 x (desired Alb - current Alb) x kg

145
Q

List Albumin products:

A

FFP = 3g/100ml

WB = 1.4g/100ml

HSA = 25g/100ml

146
Q

Transfusion volume calculations:

Transfused volume
WB
pRBC

A

Transfused volume = 90ml/donor PCV x % rise x kg

WB (PCV 45)= 2 x % rise x kg

pRBC (PCV 60) = 1.5 x % rise x kg

147
Q

Normal COP:

A

Dog 18-20
Cat 20-24

148
Q

Massive transfusion definitions:

A

More than blood volume in 24 hours

Half of BV in 3 hrs

High rate/bolus: > 1.5ml/kg/min over 20min (> 30ml/kg in 20 min)

149
Q

Metabolic acidosis compensation equation

A

0.7 DECREASE in PCO2 for each 1meq DECREASE of HCO3

150
Q

Metabolic alkalosis compensation equation

A

0.7 INCREASE in PCO2 for each 1meq INCREASE of HCO3

151
Q

Respiratory acidosis
Acute & chronic compensation equation

A

Acute: 0.15 increase HCO3 for every 1 up in pCO2

Chronic: 0.35 increase HCO3 for every 1 up in pCO2

152
Q

Respiratory alkalosis
Acute & chronic compensation equation

A

Acute: 0.25 decrease HCO3 for every 1 down in pCO2

Chronic: 0.55 decrease HCO3 for every 1 down in pCO2

153
Q

Things to remember about acid-base compensation

A
  • Compensation is always LESS than the primary problem (so a percentage = the decimal).
  • Primary problem is the 1.0.
  • Kidneys are not as good at compensating as lungs.
  • 0.15, 0.25, 0.35, 0.55 alphabetical (acute acid, acute alk, chronic acid, chronic alk)
154
Q

Henderson Hasselbach equation

A

pH = 6.1 + log HCO3 / (0.03 x pCO2)

155
Q

Bicarbonate buffer equation

A

CO2 + H20 ⟷ H2CO3 ⟷ H+ + HCO3-

CO2 + H20 ⟷ H2CO3 is mediated by carbonic anhydrase

H2CO3 ⟷ H+ + HCO3- is a fairly immediate dissociation (doesn’t hang out as H2CO3)

156
Q

Strong Ion Difference equation

A

= strong cations - strong anions

= (Na + K + Ca + Mg) - (Cl + lactate + urate

157
Q

Stewart independent variables

A
  • PCO2
  • Strong ion difference (SID= essentially Na - Cl)
  • Total weak acids (Atot = Alb + phos)
158
Q

Bicarb deficit equation

A

Meq HCO3 = kg x 0.4 x (24-patient HCO3)

24 = normal bicarb

Want to correct ¼ to ⅓ of the deficit at a time

159
Q

K shift for acid/base equation (briefly discuss)

A

0.6mEq increase in K for every 0.1 unit drop in pH

Applies to MINERAL metabolic processes only

Basically: acidosis → hyperkalemia, alkalosis → hypokalemia (use Bicarb to drop K)

160
Q

Anion Gap equation (briefly discuss)

A

= (Na + K) - (HCO3 + Cl)
= pos - neg

= essentially unmeasured anions (unmeasured cations are not variable)

Normal = 12-24

161
Q

Unmeasured acids (anions):

A

MEG’s LARK (or LARD)

Methanol
Ethylene Glycol
Salicylate
Lactic Acid
Renal acids
Ketones (DKA)

Others: Propylene Glycol, ethanol, Sulfuric acid, metaldehyde, D-lactate

162
Q

Types of lactate:

A

L-Lactate
D-Lactate

163
Q

L- Lactate

A

Animal
Produced by anaerobic metabolism

164
Q

D- Lactate

A

Bacterial

not generally measured.

Increased with short-bowel syndrome, DM, EPI, propylene glycol in cats)

165
Q

Type A Lactic acidosis

A

Tissue hypoxia

166
Q

Type B lactic acidosis

A

impaired cellular metabolism (abnormal mitochondrial dysfunction)

Congenital defect
Drugs/toxins
Lymphoma
Diabetes
Hypoglycemia
Liver/kidney failure
Sepsis

167
Q

Lactate pathway

A
168
Q

Types of ketones

A

Acetoacetate (ketostix)

Acetone

B-hydroxybutyrate (blood ketones, most abundant)

169
Q

Free water Stewart Calculation
(& effect on base excess)

A

= (Measured Na - Normal Na)/4

High Na → Alkalosis (remember- contraction alkalosis)

Low Na → Acidosis

170
Q

Chloride Stewart Calculation
(effect on base excess)

A

= Normal Cl - Corrected Cl

Remember- Hypochloremic metabolic alkalosis

Corrected Cl = measured Cl x (normal Na/measured Na)

171
Q

Corrected Cl

A

= measured Cl x (normal Na/measured Na)

172
Q

Phosphate Stewart Calculation
(effect on base excess)

A

= (Normal Phos - Measured Phos)/2

High Phos → Acidosis (Remember- renal failure acidosis)

173
Q

Albumin Stewart Calculation
(effect on base excess)

A

= (Normal Alb - Measured Alb) x 4

Low Alb → alkalosis (Remember- masks metabolic acidosis in septic patients)

174
Q

Lactate Stewart Calculation
(effect on base excess)

A

= (-1) x lactate

High lactate → acidosis

175
Q

Water = ___ % BW

A

60%

176
Q

ICF= ____ % BW

A

40% or ~(2/3)

177
Q

ECF = _______% BW

A

20 % or (1/3)

  • 3/4 interstitial (15% BW)
  • 1/4 intravascular (5% BW)
178
Q

Effects of hyperkalemia on resting membrane potential

A

increased RMP (more excitable)

179
Q

Effects of hypokalemia on resting membrane potential

A

decreased RMP (less excitable)- ie hypokalemic ventroflexion

180
Q

Effects of hypercalcemia on threshold membrane potential

A

increased TMP (less excitable)

181
Q

Effects of hypocalcemia on threshold membrane potential

A

decreased TMP (more excitable)- ie eclampsia

182
Q

Osmolarity definition

A

= # osmoles/L of solution

183
Q

Osmolality definition

A

= # osmoles/kg of solution

184
Q

Calculated Osmolality

A

=2 (Na + K) + Glu/18 + BUN/2.8

185
Q

Normal osmolality

A

~300

290-330 cat
290-310 dog

186
Q

Effective Osmolality

A

=2 (Na + K) + Glu/18

(leave out BUN- it is not an effective osmole)

187
Q

Osmole Gap:

A

= Measured Osm - Calculated Osm

Gap = unmeasured Osmoles (essentially the same as unmeasured anions)

Normal < 15

188
Q

Gibbs-Donnan Effect:

A

negatively charged proteins (albumin) attract anions (Na) which increases their effective oncotic pressure due to increased osmolarity

189
Q

Corrected Na

A

= 1.6 mEq/L drop in Na for every 100mg/dl increase in Glucose (or mannitol)

190
Q

Corrected Cl

A

= measured Cl x (normal Na/measured Na)

191
Q

Free water deficit

A

= [(Current Na/Normal Na) - 1] x 0.6 x kg

192
Q

Sodium deficit

A

= (Current Na - Normal Na) x 0.6 x kg

193
Q

Hetastarch molecular weight…

A

Lower = increased osmotic effect (more molecules/mL)

194
Q

Hetastarch degree of substitution…

A

HES = 0.7

VES = 0.4

Higher is longer lasting/more side effects.

195
Q

Hetastarch C2:C6 ratios

A

Higher lasts longer, more side effects.

More C2 is slower to hydrolyze.

196
Q

Describe Ultrafiltration in Dialysis:

A

movement of fluid (osmosis)

197
Q

Describe Diffusion in Dialysis:

A

through a membrane down a concentration gradient

198
Q

Describe convection in Dialysis:

A

movement of solutes with water flow

199
Q

Describe adsorption in Dialysis:

A

stuff binds to membrane or a special filter (ie charcoal)

200
Q

SCUF CRRT Mode:

A
  • close continuous ultrafiltration
  • just ultrafiltration (membrane, no dialysate, no replacement fluid)
201
Q

CVVH CRRT Mode:

A
  • continuous venovenous hemofiltration
  • ultrafiltration + convection (membrane + replacement fluids, no dialysate)
202
Q

CVVHD CRRT mode:

A
  • continuous venovenous hemodialysis
  • ultrafiltration + diffusion (membrane + dialysate, no replacement fluid)
203
Q

CVVHDF CRRT mode:

A
  • continuous venovenous hemodiafiltration
  • ultrafiltration, diffusion, and convection (membrane, dialysate, and replacement fluid)
204
Q

Renal Clearance equation

A

= [urine] x urine flow / [plasma]

205
Q

Renal Plasma flow equation

A

= clearance of PAH

= [PAH urine] x urine flow / [PAH plasma]

206
Q

GFR equation

A

= clearance of inulin

= [inulin urine] x urine flow / [inulin plasma]

207
Q

RBF equation

A

= RPF / (1-Hct)

208
Q

Fractional excretion (ie of Na) equation

A

FENa = (Urine Na x Plasma Creat)/ (Plasma Na x Urine Creat) x 100

209
Q

Filtration fraction equation

A

= GFR/RPF

210
Q

Excretion rate equation

A

= urine flow x [urine]

211
Q

Filtered load equation

A

= GFR x [plasma]

212
Q

Secretion rate equation

A

= excretion rate - filtered load

= (urine flow x [urine]) - (GFR x [plasma])

213
Q

Reabsorption rate equation

A

= filtered load - excretion rate

= (GFR x [plasma]) - (urine flow x [urine])

214
Q

Carbon monoxide toxicity MOA

A

competitive inhibition of O2-Hb binding (shifts Hb/O2 curve L, tighter O2 binding)

215
Q

Cyanide toxicity MOA

A

inhibits cytochrome oxidase → impaired O2 utilization by tissues.

Tx with sodium nitrate.

216
Q

Carbamates and Organophosphates toxicity MOA

A

ACH inhibition (muscarinic and nicotinic stimulation).

OP’s are irreversible
Carbamates (Tres Pasitos) are reversible.

217
Q

Bromethalin toxicity MOA

A

Uncouples oxidative phosphorylation → decreased brain ATP → pump failure/edema

218
Q

Anticoagulant rodenticides toxicity MOA

A

antagonize vitamin K epoxide reductase → inhibit carboxylation of vitamin K coag factors (2, 7, 9, 10)

219
Q

Ivermectin toxicity MOA

A

inhibits GABA gated Cl-channels in CNS (with altered BBB or OD)

220
Q

Strychnine toxicity MOA

A

inhibits the inhibitory interneurons (renshaw cells) → excitatory effect

221
Q

Metaldehyde toxicity MOA

A

Serotonin and gaba antagonist → excitatory effect

222
Q

Permethrin toxicity MOA

A

disruption of voltage/gated Na channels → early or extended depolarization

223
Q

Amitraz toxicity MOA

A

alpha agonist

224
Q

Tremorgenic mycotoxins MOA

A

Increase resting potential, increase duration of depolarization, decrease gaba → excitatory effect

225
Q

Tremorgenic mycotoxins examples

A

Penitrem A
Roquefortine
Thomitrems
Aflatrem
Verruculogen

226
Q

PPA toxicity MOA

A

Sympathomimetic (alpha and beta)

227
Q

Digitalis toxicity MOA

A

Inhibits Na/K/ATPase → increased intracellular Ca → vagal stimulation

228
Q

Ethylene glycol metabolism

A

EG → (via ADH) → glycoaldehyde → glycolate → glycoxalate → oxalate

229
Q

Ethylene glycol stages

A

Stage 1: EG induced acidosis, hyperosmolarity, ataxia/nausea (0.5-12 hrs). Need to intervene by 3 hrs in cats and 6 hrs in dogs to avoid toxic metabolites

Stage 2: Signs mostly resolve as metabolites form (8-24 hrs)

Stage 3: Acute renal failure develops from the toxic metabolites (24-72 hrs)

230
Q

Acetaminophen metabolism and toxic metabolites

A
  • Conjugated with glucuronide and sulfate
  • Unconjugated stuff gets bound to glutathione → rest is now toxic
  • NAPQI → liver toxicity mostly
  • Para-aminophenol (PAP) → Met Hb mostly
231
Q

Toxins that don’t bind charcoal

A

EG
xylitol
ethanol and other alcohols
hydrocarbons (ie petroleum)
Metals
Inorganic toxins (cyanide, ammonia, nitrates, phos, bromide)
corrosive/caustic agents
others

Boards Review (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions